subject:(CD4)

Tulane University

1. Moss, Daniel. Antigen Stability Influences Processing Efficiency and Immunogenicity of Pseudomonas Exotoxin Domain III and Ovalbumin.

Degree: 2020, Tulane University

URL: https://digitallibrary.tulane.edu/islandora/object/tulane:120437

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[email protected]

Effective adaptive immune responses depend on the presentation to CD4+ T cells antigen peptides bound to major histocompatibility complex class II proteins. The structure… (more)

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[email protected]

Effective adaptive immune responses depend on the presentation to CD4+ T cells antigen peptides bound to major histocompatibility complex class II proteins. The structure of an antigen strongly influences its processing within the endolysosome and potentially controls the identity and abundance of peptides that are presented to T cells. The dissertation presented here sought to expand our understanding of how antigen structure and stability influence adaptive immune responses for two model antigens. Pseudomonas exotoxin A domain III (PE-III) functions as an ADP-ribosyltransferase with significant cellular toxicity and has been incorporated into a recombinant immunotoxin for the treatment of cancer. The bacterial component of the PE-III immunotoxin is highly immunogenic and generates neutralizing antibodies that render subsequent treatments ineffective. A group of six single-amino-acid substitutions in PE-III that were predicted to disrupt CD4+ T-cell epitopes have been shown to reduce antibody responses in mice. Here we demonstrate that only one of the substitutions, R494A, exhibits reduced folding stability and proteolytic resistance through the removal of a hydrogen bond. This destabilization significantly reduces its antibody immunogenicity while generating CD4+ T-cell epitopes that are indistinguishable from those of wildtype PE-III. PE-III specific B cells isolated from R494A-immunized animals contained fewer somatic mutations, which are associated with affinity maturation, and exhibited a weaker germinal-center gene signature, compared to B cells from wildtype-immunized animals. Chicken ovalbumin (cOVA) has been studied for decades primarily due to the robust genetic and molecular resources that are available for experimental investigations. cOVA is a member of the serpin superfamily of proteins that function as protease inhibitors, although cOVA does not exhibit this activity. As a serpin, cOVA possess a protease-sensitive reactive center loop that lies adjacent to the OT-II epitope. We took advantage of the previously described single-substitution-variant, OVA R339T, which can undergo the dramatic structural transition observed in serpins to study how changes in loop size and protein stability influences CD4+ T-cell priming in vivo. We observed that OVA R339T loop-insertion increases overall stability and protease resistance and significantly shortens the reactive center loop. This results in reduced CD4+ T-cell priming of the OT-II epitope in SJL mice. These findings have implications for the design of more effective vaccines for the treatment of infectious diseases and cancer as well as the development of more robust CD4+ T-cell epitope prediction tools.

1

Daniel Moss

Advisors/Committee Members: Landry, Samuel (Thesis advisor), School of Medicine Biomedical Sciences Graduate Program (Degree granting institution).

Subjects/Keywords: CD4+ T cells Antigen Processing

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Moss, D. (2020). Antigen Stability Influences Processing Efficiency and Immunogenicity of Pseudomonas Exotoxin Domain III and Ovalbumin. (Thesis). Tulane University. Retrieved from https://digitallibrary.tulane.edu/islandora/object/tulane:120437

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Moss, Daniel. “Antigen Stability Influences Processing Efficiency and Immunogenicity of Pseudomonas Exotoxin Domain III and Ovalbumin.” 2020. Thesis, Tulane University. Accessed April 15, 2021. https://digitallibrary.tulane.edu/islandora/object/tulane:120437.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Moss, Daniel. “Antigen Stability Influences Processing Efficiency and Immunogenicity of Pseudomonas Exotoxin Domain III and Ovalbumin.” 2020. Web. 15 Apr 2021.

Vancouver:

Moss D. Antigen Stability Influences Processing Efficiency and Immunogenicity of Pseudomonas Exotoxin Domain III and Ovalbumin. [Internet] [Thesis]. Tulane University; 2020. [cited 2021 Apr 15]. Available from: https://digitallibrary.tulane.edu/islandora/object/tulane:120437.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Moss D. Antigen Stability Influences Processing Efficiency and Immunogenicity of Pseudomonas Exotoxin Domain III and Ovalbumin. [Thesis]. Tulane University; 2020. Available from: https://digitallibrary.tulane.edu/islandora/object/tulane:120437

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Rochester

2. Chapman, Lesley Maraina. MicroRNA-451 Regulates T Helper Cell Responses.

Degree: PhD, 2015, University of Rochester

URL: http://hdl.handle.net/1802/30109

► Background: Malaria parasite evasion of host defense mechanisms leads to uncontrolled parasite growth, anemia, morbidity, and often mortality. A number of studies have shown that… (more)

▼ Background: Malaria parasite evasion of host defense mechanisms leads to uncontrolled parasite growth, anemia, morbidity, and often mortality. A number of studies have shown that miR-451 may be a key regulator of immune function. Down regulation of miR-451 promotes the release of proinflammatory cytokines from dendritic cells, and NOTCH1 mediated repression of miR-451 promotes Tcell proliferation in a mouse leukemia model. The goal of this study is to define the underlying genetic and molecular mechanisms that lead to increased host immune responses in miR-451-/- mice during malaria infection. Results: Studies by our lab using the uncomplicated malaria mouse model of Plasmodium yoelii (P. yoelii) infection demonstrated that mice lacking miR-451 (miR-451-/-) have greatly accelerated parasite clearance compared to wild type (WT) controls. The accelerated parasite clearance is dependent on increased CD4+ T-cell proliferation responses to infection. Using RNAseq analysis we found 5028 genes were differentially expressed between WT and miR-451-/- CD4+ T cells post infection (55 genes with a log2-fold change > 2) while only 88 genes differed pre-infection. Western blot and quantitative real time PCR analysis identified increased Myc expression in miR-451-/- CD4+ T cells post infection. Myc has a key role in promoting CD4+ T-cell proliferation and our studies demonstrated that miR-451 has a negative effect CD4+ T-cell proliferation that is at least in part Myc dependent. MiR-451-/- CD4+ T cells have increased cell proliferation when stimulated in vitro compared to WT CD4+ T cells. In addition, antagomir inhibition of miR-451 in WT T cells causes an increase in WT CD4+ Tcell proliferation post stimulation in vitro. We have also shown that pharmacologic inhibition of c-myc blunts miR-451-/- CD4+ T-cell proliferation in vitro. Taken together these data indicate that miR-451 is a major regulator of CD4+ T-cell proliferation, in part via regulation of Myc expression post T-cell activation. Discussion: Our study is the first to demonstrate that the loss of a miRNA generates a protective host immune response against malaria infection. Mice lacking miR-451 have an enhanced CD4+ T-cell proliferative response post malaria infection. Decreased expression of miR-451 promotes T helper proliferation in part as a result of increased Myc expression. Among the 5028 differentially expressed genes, we have identified candidate that may be involved in cell proliferation and cytokine pathways (ie: NFKB pathway genes: Psmb8 [1.55 log2 fold change] and Ikbkb [0.72 log2 fold change]). We plan to confirm these pathways using bioinformatics analysis. This study has many clinical implications, including treating patients with miR-451 antagomirs or an adoptive cell therapy strategy in which miR-451 expression in antigen specific CD4+ T cells is blunted, and modified cells are reintroduced into the patient to enhance the CD4+ T-cell responses to malaria infection. It is also relevant to many other diseases in which…

Subjects/Keywords: CD4 T Cell; Plasmodium; MYC

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Chapman, L. M. (2015). MicroRNA-451 Regulates T Helper Cell Responses. (Doctoral Dissertation). University of Rochester. Retrieved from http://hdl.handle.net/1802/30109

Chicago Manual of Style (16^th Edition):

Chapman, Lesley Maraina. “MicroRNA-451 Regulates T Helper Cell Responses.” 2015. Doctoral Dissertation, University of Rochester. Accessed April 15, 2021. http://hdl.handle.net/1802/30109.

MLA Handbook (7^th Edition):

Chapman, Lesley Maraina. “MicroRNA-451 Regulates T Helper Cell Responses.” 2015. Web. 15 Apr 2021.

Vancouver:

Chapman LM. MicroRNA-451 Regulates T Helper Cell Responses. [Internet] [Doctoral dissertation]. University of Rochester; 2015. [cited 2021 Apr 15]. Available from: http://hdl.handle.net/1802/30109.

Council of Science Editors:

Chapman LM. MicroRNA-451 Regulates T Helper Cell Responses. [Doctoral Dissertation]. University of Rochester; 2015. Available from: http://hdl.handle.net/1802/30109

Stellenbosch University

3. Lloyd, Alexander M. Quantification of CD4+ cell count via a nanofibre-based biosensor.

Degree: MEng, Electrical and Electronic Engineering, 2019, Stellenbosch University

URL: http://hdl.handle.net/10019.1/106110

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ENGLISH ABSTRACT: Antigen-substrate binding has been found to cause a change in the resistance of conductive nanofibre substrates. This thesis endeavoured to exploit this phenomenon… (more)

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ENGLISH ABSTRACT: Antigen-substrate binding has been found to cause a change in the resistance of conductive nanofibre substrates. This thesis endeavoured to exploit this phenomenon to produce sensors capable of quantifying CD4+ cell count. Producing nanofibre substrates with appropriate robustness and reproducibility cheaply remains challenging. Previous methods coated non-conductive nanofibres with a non-uniform conductive coating or used carbon nanofibre mats that were very susceptible to mechanical stress. To address these factors that negatively affect reproducibility, intrinsically conductive nanofibres were electrospun from an organic semiconducting polymer through an adaptation of an existing method that decreased the overall material cost. The production process was tuned so as to produce mats with appropriate electrical characteristics and the fibres were aligned in a uniform direction so as to provide directed current paths. These mats were then spun directly onto interdigitated electrodes that had been printed onto semi-hydrophobic paper with silver ink via a modified inkjet printer. By employing appropriate cross-linking chemistry, antibodies were bound to the produced nanofibres. These antibodies served as the biorecognition element for the sensor. The data were analysed and it was evident that the binding event did indeed cause a change in resistance. While this resistance could not be repeatably quantified owing to base variance between electrodes, this thesis lays the groundwork for further research.

AFRIKAANSE OPSOMMING: Daar is al bevind dat antigeen-substraat binding ’n verandering veroorsaak in die weerstand van geleidende nanovesel-substrate. Hierdie tesis het gepoog om hierdie verskynsel in te span met die oog op die vervaardiging van sensors wat in staat is om CD4+ seltelling te kwantifiseer. Om nanovesel-substrate met ’n gepaste vlak van robuustheid en reproduseerbaarheid op ’n goedkoop wyse te produseer, bly ’n uitdaging. Vorige metodes het behels dat nie-geleibare nanovesels bedek word met ’n nie-uniforme geleidende laag, of het gebruik gemaak van koolstof nanovesel matte wat baie vatbaar was vir meganiese stres. Dit was noodsaaklik om hierdie faktore aan te spreek weens hul negatiewe impak op reproduseerbaarheid. Gevolglik is inherent geleidende nanovesels ge-elektrospin uit ’n organiese semi-geleidende polimeer; dit is vermag deur ’n bestaande metode aan te pas op so ’n wyse dat die kostes verbonde daaraan verlaag is. Die proses is verfyn met die doel om matte met die gepaste elektriese eienskappe te produseer en vesels wat in ’n uniforme rigting le, te vervaardig; sodoende is direkte stroompaaie geskep. Hierdie nanoveselmatte is gespin op elektrodes; die elektrodes is met silwer ink gedruk op semi-hidrofobiese papier deur middel van ’n aangepaste injet drukker. Deur die gebruik van kruisbindingchemie is teenliggaampies gebind tot die geproduseerde nanovesels. Hierdie teenliggaampies het gedien as die ”biorecognitionëlement. Uit die analise van die data…

Advisors/Committee Members: Perold, W. J., Stellenbosch University. Faculty of Engineering. Dept. of Electrical and Electronic Engineering..

Subjects/Keywords: UCTD; Nanofibers; Biosensors; CD4 antigen

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Lloyd, A. M. (2019). Quantification of CD4+ cell count via a nanofibre-based biosensor. (Thesis). Stellenbosch University. Retrieved from http://hdl.handle.net/10019.1/106110

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Lloyd, Alexander M. “Quantification of CD4+ cell count via a nanofibre-based biosensor.” 2019. Thesis, Stellenbosch University. Accessed April 15, 2021. http://hdl.handle.net/10019.1/106110.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Lloyd, Alexander M. “Quantification of CD4+ cell count via a nanofibre-based biosensor.” 2019. Web. 15 Apr 2021.

Vancouver:

Lloyd AM. Quantification of CD4+ cell count via a nanofibre-based biosensor. [Internet] [Thesis]. Stellenbosch University; 2019. [cited 2021 Apr 15]. Available from: http://hdl.handle.net/10019.1/106110.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Lloyd AM. Quantification of CD4+ cell count via a nanofibre-based biosensor. [Thesis]. Stellenbosch University; 2019. Available from: http://hdl.handle.net/10019.1/106110

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Saskatchewan

4. Rudulier, Christopher. CD4+ T cell interactions through CD28/B7 molecules affects their Th1/Th2 phenotype.

Degree: 2011, University of Saskatchewan

URL: http://hdl.handle.net/10388/ETD-2011-12-282

► The Th1/Th2 phenotype of the immune response generated against a pathogen or disease can have a profound impact upon the survival of the host. Thus,… (more)

▼ The Th1/Th2 phenotype of the immune response generated against a pathogen or disease can have a profound impact upon the survival of the host. Thus, a complete and accurate model for the generation of Th1 versus Th2 cells is critical for the development of effective immunotherapeutic strategies aimed against diseases including cancer and tuberculosis. Numerous factors are considered to be important in the differential development of Th1 and Th2 cells. These include the strength of stimulation through the T cell receptor, the cytokine environment, the dose of antigen, and the types of co-stimulatory molecules expressed by the antigen-presenting cells presenting the T cell’s cognate antigen. A common thread found in the majority of studies on the generation of Th1 and Th2 cells is that naïve CD4+ T cells are thought to be passive players in this process. In contrast, our laboratory has demonstrated, in a number of in vivo systems, that the density of the responding naïve CD4+ T cells, that is to say the frequency of responding CD4+ T cells in an animal, has a significant impact on their Th1/Th2 phenotype. In particular, our laboratory has reported that in response to antigen, a low density of responding naïve CD4+ T cells give rise to Th1 cells while a high density of responding CD4+ T cells give rise to Th2 cells. Although we have made these observations, we had not, prior to the work described herein, elucidated the mechanism(s) surrounding this phenomenon. This was the impetus for the experiments detailed in this thesis. In order to investigate the mechanism(s) mediating the effect that the density of responding CD4+ T cells has on the Th1/Th2 phenotype, we have developed an in vitro system that employs a physiological number of naïve TCR transgenic CD4+ T cells (DO11.10) specific for the OVA323-339 peptide in the context of I-Ad. My observations in this in vitro system mirror previous in vivo observation in that a low frequency of naïve CD4+ DO11.10 T cells cultured with syngeneic APC and the OVA323-339 peptide, acquire a Th1 phenotype while naïve CD4+ DO11.10 T cells cultured at high frequencies, under identical conditions, acquire a Th2 phenotype. By controlling the type of APC in our culture system, we have ascertained that the effect of CD4+ T cell density on the differential generation of Th1 and Th2 cells is mediated by B cells, but not dendritic cells. We also found that the addition of an agonistic anti-CD28 antibody skews the phenotype of T cells cultured at low densities towards the Th2 pole while partially blocking of CD80 and CD86, through the addition of CTLA4-Ig to high density T cell cultures, resulted in the development of Th1 cells. In contrast, modulating the interactions between CD40/CD40L and OX40/OX40L, two co-stimulatory molecule/ligand pairs known to affect Th1/Th2 differentiation, through the addition of agonistic and antagonistic antibodies in high or low density CD4+ T cell cultures did not alter the Th1/Th2 phenotype of the newly activated DO11.10 T cells. Thus, it appears… Advisors/Committee Members: Bretscher, Peter, Havele, Calliopi, Gerdts, Volker, Bull, Harold, Goldie, Hughes.

Subjects/Keywords: CD4 T cell differentiation

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Rudulier, C. (2011). CD4+ T cell interactions through CD28/B7 molecules affects their Th1/Th2 phenotype. (Thesis). University of Saskatchewan. Retrieved from http://hdl.handle.net/10388/ETD-2011-12-282

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Rudulier, Christopher. “CD4+ T cell interactions through CD28/B7 molecules affects their Th1/Th2 phenotype.” 2011. Thesis, University of Saskatchewan. Accessed April 15, 2021. http://hdl.handle.net/10388/ETD-2011-12-282.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Rudulier, Christopher. “CD4+ T cell interactions through CD28/B7 molecules affects their Th1/Th2 phenotype.” 2011. Web. 15 Apr 2021.

Vancouver:

Rudulier C. CD4+ T cell interactions through CD28/B7 molecules affects their Th1/Th2 phenotype. [Internet] [Thesis]. University of Saskatchewan; 2011. [cited 2021 Apr 15]. Available from: http://hdl.handle.net/10388/ETD-2011-12-282.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Rudulier C. CD4+ T cell interactions through CD28/B7 molecules affects their Th1/Th2 phenotype. [Thesis]. University of Saskatchewan; 2011. Available from: http://hdl.handle.net/10388/ETD-2011-12-282

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Addis Ababa University

5. Alem, Gebretsadik. Reducing Turnaround Time for CD4 Laboratory Test Results in Wukro Hospital .

Degree: 2013, Addis Ababa University

URL: http://etd.aau.edu.et/dspace/handle/123456789/5253

► Summary Laboratory turnaround time is defined as the length of time from when a test is ordered to the time the result is reported. Various… (more)

Subjects/Keywords: CD4 Laboratory; Test Results

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APA (6^th Edition):

Alem, G. (2013). Reducing Turnaround Time for CD4 Laboratory Test Results in Wukro Hospital . (Thesis). Addis Ababa University. Retrieved from http://etd.aau.edu.et/dspace/handle/123456789/5253

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Alem, Gebretsadik. “Reducing Turnaround Time for CD4 Laboratory Test Results in Wukro Hospital .” 2013. Thesis, Addis Ababa University. Accessed April 15, 2021. http://etd.aau.edu.et/dspace/handle/123456789/5253.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Alem, Gebretsadik. “Reducing Turnaround Time for CD4 Laboratory Test Results in Wukro Hospital .” 2013. Web. 15 Apr 2021.

Vancouver:

Alem G. Reducing Turnaround Time for CD4 Laboratory Test Results in Wukro Hospital . [Internet] [Thesis]. Addis Ababa University; 2013. [cited 2021 Apr 15]. Available from: http://etd.aau.edu.et/dspace/handle/123456789/5253.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Alem G. Reducing Turnaround Time for CD4 Laboratory Test Results in Wukro Hospital . [Thesis]. Addis Ababa University; 2013. Available from: http://etd.aau.edu.et/dspace/handle/123456789/5253

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Addis Ababa University

6. Haile, Benti. Lost opportunities to complete CD4+ T cell testing among HIV positive patients attending selected health centers in Afar region Northeast Ethiopia, 2014.

Degree: 2014, Addis Ababa University

URL: http://etd.aau.edu.et/dspace/handle/123456789/5655

► Background: In resource limited settings CD4+ T cell count (CD4 testing) facility is not available in peripheral areas and often either patients need to travel… (more)

▼ Background: In resource limited settings CD4+ T cell count (CD4 testing) facility is not available in peripheral areas and often either patients need to travel long distances or the samples need to be transported to the centers where the facility for CD4 testing is available. These results in delays in the completion of CD4 testing, and hence further delays occur in obtaining appropriate care and treatment. Objective: To estimate rates of completion of CD4+ T cell count within 12 weeks of testing positive for human immunodeficiency virus (HIV) as well as predictors for completion at ART clinics in Afar region of Northeast Ethiopia. Methods: The study was conducted in three most accessible selected Health centers with CD4 sample referring and ART services found in Afar Region of Northeast Ethiopia. Monthly report of HIV Positive patients was used to identify individuals with HIV positive results. Routine data was used separately to calculate the number and proportion of patients passing through PICHT, VCT, PMTCT, TB clinic. Of the total 1299 positive individuals at each entry point, 931 were linked to clinic patient card and ART data base. CD4 testing was considered complete once a patient had retrieved the test results. To determine the rate of CD4 testing completion, records of patient were reviewed. Predictors for completion were identified through multivariate logistic regression. SPSS version 16 was used for data cleaning and analysis. P values less than 0.05 were taken as statistically significant. Result: Between September 1, 2007 and June, 2013, a total of 1299 patients consisted of 492(37.88%), 387(29.79%), and 420(32.33%) at Gewane, Werer and Semera health centers, respectively were tested positive for HIV. Patients who initiated CD4 testing after they tested positive for HIV and enrolled to ART clinic had a median CD4 cell count of 172/μl (interquartile range, IQR: 88–261). Majority 326 (59.8% of 545) had a CD4 cell count ≤ 200/μl and were already eligible for ART. The other 219 (40.2% of 545) had a CD4 cell count > 200/μl and were thus eligible for pre-ART medical care. Of the 931 patients who were included in the study, 58.5% initiated CD4 testing within the 12 weeks study timeframe. Of these patients, 59.8% were immediately eligible for antiretroviral therapy (ART) because of a CD4 cell count ≤ 200/μl, but only 42.9% of the patients in this ix category completed CD4 testing within 12 weeks of HIV testing. Among those not immediately eligible for ART (CD4 cells > 200/μl), only 31.5% completed CD4 testing within 12 weeks. Overall, of HIV+ patients who initiated CD4 testing, 61.65% did not complete it within 12 weeks of diagnosis. Among the predicting factors, the higher the baseline CD4 cell count, the lower the odds of completing CD4 testing within 12 weeks (P<0.05). Conclusion: Majority of patients were already eligible for ART at the time of HIV diagnosis even under the restrictive threshold of 200 CD4 cells/μl that prevailed at the time of the study. But most did not complete CD4 testing within… Advisors/Committee Members: Aster Tsegaye (MSc, PhD), Fatuma Hassen(BSc, MPH) (advisor).

Subjects/Keywords: CD4+ T cell count; HIV

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Haile, B. (2014). Lost opportunities to complete CD4+ T cell testing among HIV positive patients attending selected health centers in Afar region Northeast Ethiopia, 2014. (Thesis). Addis Ababa University. Retrieved from http://etd.aau.edu.et/dspace/handle/123456789/5655

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Haile, Benti. “Lost opportunities to complete CD4+ T cell testing among HIV positive patients attending selected health centers in Afar region Northeast Ethiopia, 2014. ” 2014. Thesis, Addis Ababa University. Accessed April 15, 2021. http://etd.aau.edu.et/dspace/handle/123456789/5655.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Haile, Benti. “Lost opportunities to complete CD4+ T cell testing among HIV positive patients attending selected health centers in Afar region Northeast Ethiopia, 2014. ” 2014. Web. 15 Apr 2021.

Vancouver:

Haile B. Lost opportunities to complete CD4+ T cell testing among HIV positive patients attending selected health centers in Afar region Northeast Ethiopia, 2014. [Internet] [Thesis]. Addis Ababa University; 2014. [cited 2021 Apr 15]. Available from: http://etd.aau.edu.et/dspace/handle/123456789/5655.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Haile B. Lost opportunities to complete CD4+ T cell testing among HIV positive patients attending selected health centers in Afar region Northeast Ethiopia, 2014. [Thesis]. Addis Ababa University; 2014. Available from: http://etd.aau.edu.et/dspace/handle/123456789/5655

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Montana

7. Osborne, Douglas Grant. Biological effects of trogocytosis on CD4+ T lymphocytes.

Degree: PhD, 2013, University of Montana

URL: https://scholarworks.umt.edu/etd/100

► Antigen recognition by CD4+ T cells leads to large-scale spatial and temporal molecular redistributions, forming the immunological synapse. We have previously shown that upon… (more)

Subjects/Keywords: T cells; trogocytosis; CD4; imaging

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APA (6^th Edition):

Osborne, D. G. (2013). Biological effects of trogocytosis on CD4+ T lymphocytes. (Doctoral Dissertation). University of Montana. Retrieved from https://scholarworks.umt.edu/etd/100

Chicago Manual of Style (16^th Edition):

Osborne, Douglas Grant. “Biological effects of trogocytosis on CD4+ T lymphocytes.” 2013. Doctoral Dissertation, University of Montana. Accessed April 15, 2021. https://scholarworks.umt.edu/etd/100.

MLA Handbook (7^th Edition):

Osborne, Douglas Grant. “Biological effects of trogocytosis on CD4+ T lymphocytes.” 2013. Web. 15 Apr 2021.

Vancouver:

Osborne DG. Biological effects of trogocytosis on CD4+ T lymphocytes. [Internet] [Doctoral dissertation]. University of Montana; 2013. [cited 2021 Apr 15]. Available from: https://scholarworks.umt.edu/etd/100.

Council of Science Editors:

Osborne DG. Biological effects of trogocytosis on CD4+ T lymphocytes. [Doctoral Dissertation]. University of Montana; 2013. Available from: https://scholarworks.umt.edu/etd/100

University of Montana

8. Reed, Steven James. Impacts of Trogocytosis-Mediated Intracellular Signaling on CD4+ T cell Effector Cytokine Production and Differentiation.

Degree: PhD, 2019, University of Montana

URL: https://scholarworks.umt.edu/etd/11453

► Trogocytosis is the direct intercellular transfer of membrane and membrane associated molecules. Unlike other passive-membrane transfer events, trogocytosed molecules may remain fully functional and… (more)

▼ Trogocytosis is the direct intercellular transfer of membrane and membrane associated molecules. Unlike other passive-membrane transfer events, trogocytosed molecules may remain fully functional and become re-expressed on the surface of the trogocytosis-positive (trog+) recipient. This phenomenon commonly occurs between various cell types, including those of the immune system. CD4+ T cell trogocytosis occurs during their activation by antigen presenting cells (APC). Consequently, the acquired molecules include ligands for signaling receptors on the T cell. The impacts of CD4+ trogocytosis on the immune response are largely unknown. While it has been demonstrated that trog+ cells can present trogocytosed peptide:MHC (pMHC), and costimulatory molecules to activate other T cells, the consequences of trogocytosis on the individual trog+ CD4+ T cell have not been studied in-depth. We previously reported that trog+ cells perform cell-autonomous signaling by trogocytosed ligands engaging surface receptors, referred here to as trogocytosis-mediated signaling. This signaling led to the enhanced survival of trog+ cells in vitro compared to trog– cells after APC removal. Because the duration of T cell signaling influences the activation, lineage determination, and effector functionality of CD4+ T cells; trogocytosis-mediated signaling has the potential to uniquely modulate the effector-cytokine production and differentiation of trog+ CD4+ T cell after separation from APC. Examining this possibility is the foundation for this dissertation. Here, I will report my findings that: 1. Between 0-72 hrs post-separation from APC, trogocytosis-mediated signaling drives IL-4 and GATA-3 expression, consistent with T helper type-2 (TH2) differentiation; 3. Extended trogocytosis-mediated signaling (>72 hrs) leads to the expression of Bcl-6, PD-1, CXCR5, and IL-21, consistent with T follicular helper (TFH) differentiation; 4. In absence of exogenous antigen (Ag), trogocytosis-mediated signaling is critical for the survival of the activated CD4+ T cells with high memory-potential. Despite the critical role for CD4+ T cells in generating protective immunity in the host, much remains unknown about the differentiation of CD4+ T cell effector subsets. The findings here present a novel mechanism for CD4+ T cell activation and differentiation via trogocytosis-mediated signaling, demonstrating the broad implications for such signaling in matters of public health.

Subjects/Keywords: CD4+; Differentiation; Signaling; Trogocytosis

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Reed, S. J. (2019). Impacts of Trogocytosis-Mediated Intracellular Signaling on CD4+ T cell Effector Cytokine Production and Differentiation. (Doctoral Dissertation). University of Montana. Retrieved from https://scholarworks.umt.edu/etd/11453

Chicago Manual of Style (16^th Edition):

Reed, Steven James. “Impacts of Trogocytosis-Mediated Intracellular Signaling on CD4+ T cell Effector Cytokine Production and Differentiation.” 2019. Doctoral Dissertation, University of Montana. Accessed April 15, 2021. https://scholarworks.umt.edu/etd/11453.

MLA Handbook (7^th Edition):

Reed, Steven James. “Impacts of Trogocytosis-Mediated Intracellular Signaling on CD4+ T cell Effector Cytokine Production and Differentiation.” 2019. Web. 15 Apr 2021.

Vancouver:

Reed SJ. Impacts of Trogocytosis-Mediated Intracellular Signaling on CD4+ T cell Effector Cytokine Production and Differentiation. [Internet] [Doctoral dissertation]. University of Montana; 2019. [cited 2021 Apr 15]. Available from: https://scholarworks.umt.edu/etd/11453.

Council of Science Editors:

Reed SJ. Impacts of Trogocytosis-Mediated Intracellular Signaling on CD4+ T cell Effector Cytokine Production and Differentiation. [Doctoral Dissertation]. University of Montana; 2019. Available from: https://scholarworks.umt.edu/etd/11453

University of Rochester

9. Sojka, Dorothy Katherine. Control of CD4+ T Cell Function by CD4+CD25+ Regulatory T Cells.

Degree: PhD, 2009, University of Rochester

URL: http://hdl.handle.net/1802/8161

► In the periphery thymus derived, naturally occurring CD4+CD25+Foxp3+ (Treg(s)) have the potential to suppress an extensive array of immune responses that exceed their original identification… (more)

▼ In the periphery thymus derived, naturally occurring CD4+CD25+Foxp3+ (Treg(s)) have the potential to suppress an extensive array of immune responses that exceed their original identification of preventing autoimmune disease. In recent years Treg mediated beneficial and harmful suppressive activities have been attributed to limiting responses to infectious agents and tumor antigens, respectively. In various immune settings Tregs have been implicated in controlling initial T cell activation, proliferation, differentiation, effector function, and migration. Although Tregs have an extensive suppressive agenda, their mechanisms of action are not well understood. Costimulatory signals from CD28 and CTLA-4 have been identified to regulate both target T cells and Tregs and can either help the cell escape suppression or mediate the suppression. This thesis will focus on the CD4+ effector functions that are modified by Tregs in the presence of CD28 signaling as well as the role of CTLA-4 in Treg function. To get a better understanding of Treg action we first investigated the kinetics of murine Treg activity in vitro. Tregs were suppressive within a surprisingly narrow kinetic window: necessary and sufficient only in the first 6-10h of culture. Importantly, the timing of suppression was dictated by the kinetics of target T cell activation suggesting that early target T cell signals may alter susceptibility to suppression. CD28 signals enabled target T cells to resist the early Treg-induced downregulation of IL-2. Disabling one mode of Treg suppressive activity, IL-2 secretion and proliferation, by provision of CD28 allowed us to test other arms of Treg suppressive activities. Here we define specific requirements for suppression of IL-2 secretion and proliferation than that for suppression of IFN- secretion. CD28 signaling abrogates Treg action through rendering the target T cell resistant to Treg suppression. We reveal that while CD28 signals do bypass the Treg blockade of IL-2 secretion and proliferation, the target cells remain susceptible to Treg suppression of IFN- secretion. Early during priming, secretion of IFN- by proliferating CD4+ T cells is suppressed by Tregs. This acute shutoff of effector cytokine production is IL-10 dependent but independent of TGF-. The Treg source of IL-10 suppresses IFN- secretion but plays no role in suppressing IL-2 secretion and proliferation. In addition, Tregs from p35 KO and p40 KO mice fail to suppress IFN- secretion but do not lose their ability to suppress IL-2 secretion and proliferation. Thus, Tregs use a distinct set of suppressive factors for the regulation of IL-2 secretion and proliferation than for effector cytokine production. The loss of Treg function in the absence of IL-10, p35 and p40 suggests that either these molecules are part of the Treg suppressive arsenal, or perhaps more interestingly, that they are required to ‘condition’ Tregs to gain suppressive function for IFN-. In a separate set of in vivo experiments we set out to test the contributions of a…

Subjects/Keywords: TREGS; CD4; Differentiation; CD4+CD25+

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Sojka, D. K. (2009). Control of CD4+ T Cell Function by CD4+CD25+ Regulatory T Cells. (Doctoral Dissertation). University of Rochester. Retrieved from http://hdl.handle.net/1802/8161

Chicago Manual of Style (16^th Edition):

Sojka, Dorothy Katherine. “Control of CD4+ T Cell Function by CD4+CD25+ Regulatory T Cells.” 2009. Doctoral Dissertation, University of Rochester. Accessed April 15, 2021. http://hdl.handle.net/1802/8161.

MLA Handbook (7^th Edition):

Sojka, Dorothy Katherine. “Control of CD4+ T Cell Function by CD4+CD25+ Regulatory T Cells.” 2009. Web. 15 Apr 2021.

Vancouver:

Sojka DK. Control of CD4+ T Cell Function by CD4+CD25+ Regulatory T Cells. [Internet] [Doctoral dissertation]. University of Rochester; 2009. [cited 2021 Apr 15]. Available from: http://hdl.handle.net/1802/8161.

Council of Science Editors:

Sojka DK. Control of CD4+ T Cell Function by CD4+CD25+ Regulatory T Cells. [Doctoral Dissertation]. University of Rochester; 2009. Available from: http://hdl.handle.net/1802/8161

Universidade Federal da Bahia

10. Ana Luiza Dias Angelo. Evaluating the total lymphocyte count (TLC) as a substitute for CD4 cell count in the follow up of AIDS patients.

Degree: 2005, Universidade Federal da Bahia

URL: http://www.bibliotecadigital.ufba.br/tde_busca/arquivo.php?codArquivo=2023

►

CD4 count is the major surrogate marker for defining the best time to start antiretroviral therapy in HIV infected patients, as well as for defining… (more)

▼

CD4 count is the major surrogate marker for defining the best time to start antiretroviral therapy in HIV infected patients, as well as for defining the duration of prophylaxis against opportunistic infection. Its high cost, however, limits the use of this technique in resource-limited settings. Total lymphocyte count (TLC) has been evaluated as a substitute marker for CD4 count. The objective of this study is to evaluate the capability of TLC to be used as a substitute marker for CD4 count in order to detect patients who need prophylaxis against opportunistic infection (CD4 <200 cells/mm3), and those with CD4 <350 cells/mm3 (Brazilian limit to define AIDS). We evaluated TLC and CD4 of 1174 HIV-infected patients, in HUPES, from May/2003 to September/2004. CD4 counts were performed by flow cytometry, and TLC by an automated hematological counter. A total of 1510 subjects were evaluated. The CD4 count range was 4 to 2531 cells/mm3), and the TLC range 300 to 6200 cells/mm3. The best TLC limit to estimate a CD4 <200 cells/mm3 was ≤ 1700 cells/mm3 (SE= 76.3%; SPE= 65.2%, NPV= 93.1%), but the PPV was only 31.1%. The same findings were observed for the limit of <350 cells/mm3, but we find a worst sensitivity (SE= 59.4%, SPE= 96.6%, PPV= 57.3% and NPV= 79.4%). Altogether, these results indicates that although a statistical correlation exists between TLC and the CD4+ T cell count, the TLC is not a good predictor of the CD4+ T cell count. TLC would not be a safe marker for a CD4+ T cell count in HIV-infected patients, but could be used as an surrogate to monitoring the need to perform CD4 cell count.

A contagem de células T CD4+ é o principal marcador imunológico usado para definir o momento adequado para início da terapia antiretroviral e profilaxia para infecções oportunistas em pacientes portadores do vírus HIV. Seu alto custo limita o uso desta técnica em muitos locais no mundo. O objetivo deste estudo foi avaliar a utilidade da TLC em substituir a contagem de células T CD4+ como marcador imunológico para detectar os pacientes com necessidade de profilaxia contra infecções oportunistas (CD4 <200 cel/mm3), e aqueles com CD4 <350 cel/mm3 (limite brasileiro que define AIDS). Nós analisamos a TLC e contagem de células T CD4 de 1174 pacientes infectados pelo HIV provenientes do HUPES durante o período de maio/2003 a setembro/2004. A contagem de células T CD4+ foi realizada por citometria de fluxo e a contagem total de linfócitos por contador hematológico automatizado. Foram analisadas um total de 1510 amostras. A contagem de células T CD4+ teve valor mínimo de 4 cel/mm3 e valor máximo de 2531 cel/mm3, TLC teve mínimo de 300 cel/mm3 e máximo de 6200 cel/mm3. O melhor valor de TLC, capaz de predizer CD4 <200 cel/mm3, foi ≤ 1700 cel/mm3 (SE=76,3%; SPE=65,2%, NPV=93,1%), mas PPV de somente 31,1%. Resultados semelhantes foram encontrados para contagem de células T CD4+ <350 cel/mm3, entretanto observou-se menor sensibilidade (SE= 59,4%, SPE=96,6%, PPV= 57,3% e NPV= 79,4%). Estes resultados indicam que apesar da forte…

Advisors/Committee Members: Eduardo Martins Netto, Theolis Costa Barbosa Bessa, Carlos Roberto Brites Alves.

Subjects/Keywords: CD4; TLC; AIDS; HIV; imunologia celular; IMUNOLOGIA; TLC; CD4

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Angelo, A. L. D. (2005). Evaluating the total lymphocyte count (TLC) as a substitute for CD4 cell count in the follow up of AIDS patients. (Thesis). Universidade Federal da Bahia. Retrieved from http://www.bibliotecadigital.ufba.br/tde_busca/arquivo.php?codArquivo=2023

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Angelo, Ana Luiza Dias. “Evaluating the total lymphocyte count (TLC) as a substitute for CD4 cell count in the follow up of AIDS patients.” 2005. Thesis, Universidade Federal da Bahia. Accessed April 15, 2021. http://www.bibliotecadigital.ufba.br/tde_busca/arquivo.php?codArquivo=2023.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Angelo, Ana Luiza Dias. “Evaluating the total lymphocyte count (TLC) as a substitute for CD4 cell count in the follow up of AIDS patients.” 2005. Web. 15 Apr 2021.

Vancouver:

Angelo ALD. Evaluating the total lymphocyte count (TLC) as a substitute for CD4 cell count in the follow up of AIDS patients. [Internet] [Thesis]. Universidade Federal da Bahia; 2005. [cited 2021 Apr 15]. Available from: http://www.bibliotecadigital.ufba.br/tde_busca/arquivo.php?codArquivo=2023.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Angelo ALD. Evaluating the total lymphocyte count (TLC) as a substitute for CD4 cell count in the follow up of AIDS patients. [Thesis]. Universidade Federal da Bahia; 2005. Available from: http://www.bibliotecadigital.ufba.br/tde_busca/arquivo.php?codArquivo=2023

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

11. Thiago Aparecido da Silva. Efeito da lectina ArtinM sobre as células T CD4+ murinas.

Degree: 2012, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/17/17136/tde-31082016-114033/

► A lectina ArtinM, extraída de sementes de Artocarpus heterophyllus e caracterizada como um homotetrâmero constituído de subunidades de 16 kDa, tem alta afinidade de ligação… (more)

▼ A lectina ArtinM, extraída de sementes de Artocarpus heterophyllus e caracterizada como um homotetrâmero constituído de subunidades de 16 kDa, tem alta afinidade de ligação a manotriose Man? 1-3 [Man? 1-6] Man, que constitui o core de N-glicanas. ArtinM é dotada de interessantes propriedades biológicas: (1) ativa neutrófilos a partir do reconhecimento de N-glicanas dos receptores CXCR2 e TLR2; (2) induz a desgranulação de mastócitos por interagir com N-glicanas de Fc?R ou com N-glicanas de IgE ligadas a Fc?R; (3) estimula a produção de IL-12, por reconhecer N-glicanas contidas no ectodomínio de TLR2 da superfície de células apresentadoras de antígeno (APCs); (4) exerce atividade imunomoduladora, que direciona o padrão de resposta para o perfil Th1; (5) confere resistência a infecções por patógenos intracelulares, como Paracoccidioides brasiliensis, Leishmania amazonensis e Leishmania major, Neospora caninum e Candida albicans Células T CD4+ participam de funções essenciais do sistema imune; durante o estabelecimento de uma resposta imune, podem ser desenvolvidas subpopulações de células T CD4+ adequadas para gerar respostas eficientes de combate a patógenos, manutenção da tolerância e regulação da imunidade. A ativação das células T CD4+ depende de um primeiro sinal, desencadeado pelo complexo TCR/CD3, e de um segundo sinal, oriundo de moléculas coestimulatórias como CD28. A ativação e expansão de células T CD4+ são limitadas pela ação de moléculas inibitórias, principalmente por CTLA-4. Lectinas podem ativar as células T, sendo a fitohemaglutinina (PHA) e a Concanavalin A (ConA) os exemplos mais conhecidos. Além disso, está bem caracterizado que o alvo de reconhecimento de ConA localiza-se no complexo TCR/CD3. No presente estudo buscou-se caracterizar os efeitos da lectina ArtinM sobre células T CD4+ murinas e investigar os possíveis mecanismos responsáveis pelos efeitos exercidos. Foram avaliados, inicialmente, os efeitos diretos de ArtinM sobre as células T CD4+, no que se refere à produção de citocinas, expressão de moléculas coestimulatórias e inibitórias e indução de diferenciação celular. Passou-se então à identificação de possíveis receptores de superfície reconhecidos por ArtinM e responsáveis pelo desencadeamento da ativação celular. Finalmente, buscou-se apontar moléculas sinalizadoras envolvidas nos efeitos diretos de ArtinM. A primeira evidência da interação direta de ArtinM com células T CD4+ foi proporcionada por aglutinação celular. Uma curva dose-resposta revelou que 5µg/ml foi a melhor concentração para adquirir significativa produção de citocinas Th1 (IL-2 e IFN-?) e Th17 (IL-6 e IL-17A) pelas células T CD4+. O estímulo com a concentração ótima de ArtinM mostrou que após 12 horas de incubação houve um significativo aumento nos níveis de IL-2, IFN-?, IL-6 e IL-17A no sobrenadante celular; persistindo no curso de 48 horas de observação. A secreção concomitante de IFN-? e IL-17A motivou a avaliação, por citometria de fluxo, da ocorrência de dupla marcação intracelular dessas citocinas. O estímulo, por… Advisors/Committee Members: Maria Cristina Roque Antunes Barreira, Vania Luiza Deperon Bonato, Roger Chammas.

Subjects/Keywords: ArtinM; Células T CD4+; Lectinas; ArtinM; CD4+ T cell; Lectin

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Silva, T. A. d. (2012). Efeito da lectina ArtinM sobre as células T CD4+ murinas. (Masters Thesis). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/17/17136/tde-31082016-114033/

Chicago Manual of Style (16^th Edition):

Silva, Thiago Aparecido da. “Efeito da lectina ArtinM sobre as células T CD4+ murinas.” 2012. Masters Thesis, University of São Paulo. Accessed April 15, 2021. http://www.teses.usp.br/teses/disponiveis/17/17136/tde-31082016-114033/.

MLA Handbook (7^th Edition):

Silva, Thiago Aparecido da. “Efeito da lectina ArtinM sobre as células T CD4+ murinas.” 2012. Web. 15 Apr 2021.

Vancouver:

Silva TAd. Efeito da lectina ArtinM sobre as células T CD4+ murinas. [Internet] [Masters thesis]. University of São Paulo; 2012. [cited 2021 Apr 15]. Available from: http://www.teses.usp.br/teses/disponiveis/17/17136/tde-31082016-114033/.

Council of Science Editors:

Silva TAd. Efeito da lectina ArtinM sobre as células T CD4+ murinas. [Masters Thesis]. University of São Paulo; 2012. Available from: http://www.teses.usp.br/teses/disponiveis/17/17136/tde-31082016-114033/

University of Zambia

12. Chimanuka, Ganywamulume Dominique. Association between Clinical Stages (WHO) and CD4+T-Cell count in HIV infected adults at University Teaching Hospital in Lusaka,Zambia .

Degree: 2012, University of Zambia

URL: http://hdl.handle.net/123456789/983

► Infection with HIV ultimately results in profound immunodeficiency, in which patients may present with various AIDS – defining clinical conditions.The CD4+T-cell count is an important… (more)

▼ Infection with HIV ultimately results in profound immunodeficiency, in which patients may present with various AIDS – defining clinical conditions.The CD4+T-cell count is an important parameter to understand HIV-related opportunistic infections. In poor countries and populations with limited resources, WHO staging system may more useful than CDC classification system of HIV infection. This study was conducted to examine the relationship between WHO clinical stages and CD4+T-cell count in HIV-infected adults at UTH in Lusaka, Zambia. Selected HIV-infected Zambians adults attending UTH were examined and categorized in WHO clinical stages in a cross-sectional study. Blood was collected for CD4+T-cell count using the FACS method. Different models were developed for the distribution of CD4+T-cell count with other variables. The mean CD4+T-cell counts were estimated and compared between WHO clinical stages. We utilised Epi –Info 6 for descriptive and bi -variable analysis with linear regression for correlation.Of 216 HIV participants of the study, 107 (49.5%) were males and 109 (50.5%) females. The mean BMI was estimated at 21.2kg/m2 for the all study population and 44 (23.3%), 16 (8.5%), 83 (43.9%) and 46 (24.3%) subjects were in stage 1, 2, 3 and 4 respectively. Pulmonary tuberculosis (19%), severe bacterial infection (9.7%), weight loss > 10% (7.4%) and oral candidiasis (6.7%) were the commonest clinical conditions diagnosed among symptomatic participants.One hundred three (55.7 %) participants had CD4+T-cell count less than 200 and only 27 (14.6%) of them were in stage 4. Among all individuals of the study, 83 (43.9%) and 46 (24.3 %) were in stage 3 and 4 respectively.In conclusion, this hospital-based cross-sectional study showed a weak correlation between clinical stages of the WHO Staging system and the CD4 + T-Cell Count in adult Zambian HIV-infected patients at UTH. The majority of the patients observed were in stages 3 and 4, of the WHO Staging system and half of the study population had low CD4 +T-Cell Count (less than 200 cells/ul). A larger population-based study including asymptomatic patients with higher CD4 counts would be useful to confirm the findings of this study and help health authorities with formulation of policies and projection of costs of provision of lifelong treatment.

Subjects/Keywords: CD4+T-Cell Count – HIV Adults

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Chimanuka, G. D. (2012). Association between Clinical Stages (WHO) and CD4+T-Cell count in HIV infected adults at University Teaching Hospital in Lusaka,Zambia . (Thesis). University of Zambia. Retrieved from http://hdl.handle.net/123456789/983

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Chimanuka, Ganywamulume Dominique. “Association between Clinical Stages (WHO) and CD4+T-Cell count in HIV infected adults at University Teaching Hospital in Lusaka,Zambia .” 2012. Thesis, University of Zambia. Accessed April 15, 2021. http://hdl.handle.net/123456789/983.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Chimanuka, Ganywamulume Dominique. “Association between Clinical Stages (WHO) and CD4+T-Cell count in HIV infected adults at University Teaching Hospital in Lusaka,Zambia .” 2012. Web. 15 Apr 2021.

Vancouver:

Chimanuka GD. Association between Clinical Stages (WHO) and CD4+T-Cell count in HIV infected adults at University Teaching Hospital in Lusaka,Zambia . [Internet] [Thesis]. University of Zambia; 2012. [cited 2021 Apr 15]. Available from: http://hdl.handle.net/123456789/983.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Chimanuka GD. Association between Clinical Stages (WHO) and CD4+T-Cell count in HIV infected adults at University Teaching Hospital in Lusaka,Zambia . [Thesis]. University of Zambia; 2012. Available from: http://hdl.handle.net/123456789/983

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Ruhr Universität Bochum

13. Nabi, Ghulam. Differential regulation of humoral immune responses to Gag and Env proteins of Simian Immunodeficiency Virus (SIV).

Degree: 2008, Ruhr Universität Bochum

URL: http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-24335

► Im Gegensatz zum Rückgang der Gag-spezifischen Antikörperantwort nach Einsetzen der klinischen Phase von HIV und dem Verlust von CD4+ T-Zellen bleiben die env-spezifischen Antikörper erhalten,… (more)

Subjects/Keywords: T-Lymphozyt; Antikörper; Antigen CD4; Regulation

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APA (6^th Edition):

Nabi, G. (2008). Differential regulation of humoral immune responses to Gag and Env proteins of Simian Immunodeficiency Virus (SIV). (Thesis). Ruhr Universität Bochum. Retrieved from http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-24335

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Nabi, Ghulam. “Differential regulation of humoral immune responses to Gag and Env proteins of Simian Immunodeficiency Virus (SIV).” 2008. Thesis, Ruhr Universität Bochum. Accessed April 15, 2021. http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-24335.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Nabi, Ghulam. “Differential regulation of humoral immune responses to Gag and Env proteins of Simian Immunodeficiency Virus (SIV).” 2008. Web. 15 Apr 2021.

Vancouver:

Nabi G. Differential regulation of humoral immune responses to Gag and Env proteins of Simian Immunodeficiency Virus (SIV). [Internet] [Thesis]. Ruhr Universität Bochum; 2008. [cited 2021 Apr 15]. Available from: http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-24335.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Nabi G. Differential regulation of humoral immune responses to Gag and Env proteins of Simian Immunodeficiency Virus (SIV). [Thesis]. Ruhr Universität Bochum; 2008. Available from: http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-24335

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

14. Doe, Henrietta Terko. Expression of PD-1/LAG-3 and cytokine production by CD4+T cells during infection with Plasmodiumparasites : マラリア原虫感染におけるCD４＋T細胞のPD-1／LAG-3発現とサイトカイン産生の解析.

Degree: 博士(医学), 2016, Nagasaki University / 長崎大学

URL: http://hdl.handle.net/10069/37062

► CD4+ T cells play critical roles in protection against the blood-stage of malaria infection, but their uncontrolled activation can be harmful to the host. We… (more)

Subjects/Keywords: malaria; CD4+ T cells; inhibitory receptor; cytokines

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APA (6^th Edition):

Doe, H. T. (2016). Expression of PD-1/LAG-3 and cytokine production by CD4+T cells during infection with Plasmodiumparasites : マラリア原虫感染におけるCD４＋T細胞のPD-1／LAG-3発現とサイトカイン産生の解析. (Thesis). Nagasaki University / 長崎大学. Retrieved from http://hdl.handle.net/10069/37062

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Doe, Henrietta Terko. “Expression of PD-1/LAG-3 and cytokine production by CD4+T cells during infection with Plasmodiumparasites : マラリア原虫感染におけるCD４＋T細胞のPD-1／LAG-3発現とサイトカイン産生の解析.” 2016. Thesis, Nagasaki University / 長崎大学. Accessed April 15, 2021. http://hdl.handle.net/10069/37062.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Doe, Henrietta Terko. “Expression of PD-1/LAG-3 and cytokine production by CD4+T cells during infection with Plasmodiumparasites : マラリア原虫感染におけるCD４＋T細胞のPD-1／LAG-3発現とサイトカイン産生の解析.” 2016. Web. 15 Apr 2021.

Vancouver:

Doe HT. Expression of PD-1/LAG-3 and cytokine production by CD4+T cells during infection with Plasmodiumparasites : マラリア原虫感染におけるCD４＋T細胞のPD-1／LAG-3発現とサイトカイン産生の解析. [Internet] [Thesis]. Nagasaki University / 長崎大学; 2016. [cited 2021 Apr 15]. Available from: http://hdl.handle.net/10069/37062.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Doe HT. Expression of PD-1/LAG-3 and cytokine production by CD4+T cells during infection with Plasmodiumparasites : マラリア原虫感染におけるCD４＋T細胞のPD-1／LAG-3発現とサイトカイン産生の解析. [Thesis]. Nagasaki University / 長崎大学; 2016. Available from: http://hdl.handle.net/10069/37062

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

15. Stienne, Caroline. Rôle du facteur de transcription Foxo3 dans la différenciation des LT CD4+ et la susceptibilité à l'auto-immunité : Foxo3 controls CD4 T cell differentiation and suscptibility of autoimmunity.

Degree: Docteur es, Immunologie, 2015, Université Toulouse III – Paul Sabatier

URL: http://www.theses.fr/2015TOU30284

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Le facteur de transcription Foxo3 régule la progression du cycle cellulaire, la survie cellulaire ou encore la réparation de l'ADN. En plus de ses fonctions… (more)

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Le facteur de transcription Foxo3 régule la progression du cycle cellulaire, la survie cellulaire ou encore la réparation de l'ADN. En plus de ses fonctions de gène suppresseur de tumeur, de nombreuses études ont montré le rôle crucial de Foxo3 dans les cellules du système immunitaire en particulier les cellules dendritiques ou encore les LT CD8+ dans un contexte d'infection virale. Cependant, le rôle de Foxo3 dans les LT CD4+ n'est pas encore bien connu. Ainsi, mon projet de thèse s'est intéressé à analyser le rôle de Foxo3 dans le compartiment T CD4+ dans un modèle animal d'auto-immunité. Mes résultats de Thèse montrent que le niveau d'expression de Foxo3 dans les LT CD4+ est dépendant de la force du signal reçu par le récepteur T. De plus, suite à l'activation des LT CD4+ in vitro, nous avons montré que les LT CD4+ déficients pour Foxo3 présentent un défaut de production d'IFN-? et de GM-CSF. La dissection des mécanismes moléculaires impliqués nous a permis d'identifier une nouvelle cible transcriptionnelle directe de Foxo3, le facteur de transcription Eomes, connu comme étant impliqué dans la production d'IFN-? par les LT CD8+ et identifié comme un gène de susceptibilité à la sclérose en plaques. Afin d'étudier le rôle de Foxo3 dans l'auto-immunité nous avons utilisé le modèle murin de sclérose en plaque, l'encéphalomyélite auto-immune expérimentale ou EAE. Nous avons observé que les souris déficientes pour Foxo3 développent une EAE significativement moins sévère que les souris contrôles et que cette diminution de sévérité est associée à un défaut de production d'IFN-? et de GM-CSF par les LT CD4+. Ainsi ces résultats montrent pour la première fois que Foxo3 joue un rôle crucial dans le compartiment T CD4+ et révèlent le rôle essentiel de l'axe Foxo3-Eomes dans la différentiation des LT CD4+ effecteurs et dans la susceptibilité à l'inflammation du système nerveux central.

Foxo3 transcription factor regulates cell cycle progression, survival and DNA repair pathways. In addition to its role as a tumor suppressor gene, studies have established the crucial role of Foxo3 in immune cells, notably in dendritic cells and CD8+ T cells in the context of a viral infection. However, the role of Foxo3 in CD4+ T cell function is still unknown. My PhD project was therefore to address the role of Foxo3 in CD4+ T cell biology and its role in the pathophysiology of autoimmunity. Results obtained during my PhD showed that Foxo3 expression level in CD4+ T cells is dynamically controlled by T-cell receptor signaling strength and that, after in vitro stimulation, Foxo3-deficient CD4+ T cells exhibited decreased secretion of IFN-? and GM-CSF. By dissecting the underlying molecular mechanisms, we have identified a new direct target gene of Foxo3, the transcription factor Eomes, known to be involved in IFN-? production by CD8+ T cells and as a susceptibility gene for multiple sclerosis. This led us to hypothesize that Foxo3 could be involved in the susceptibility to central nervous system inflammation. To test this hypothesis, we used…

Advisors/Committee Members: Dejean, Anne (thesis director), Saoudi, Abdelhadi (thesis director).

Subjects/Keywords: Foxo3; Différenciation; LT CD4; Auto-immunité

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Stienne, C. (2015). Rôle du facteur de transcription Foxo3 dans la différenciation des LT CD4+ et la susceptibilité à l'auto-immunité : Foxo3 controls CD4 T cell differentiation and suscptibility of autoimmunity. (Doctoral Dissertation). Université Toulouse III – Paul Sabatier. Retrieved from http://www.theses.fr/2015TOU30284

Chicago Manual of Style (16^th Edition):

Stienne, Caroline. “Rôle du facteur de transcription Foxo3 dans la différenciation des LT CD4+ et la susceptibilité à l'auto-immunité : Foxo3 controls CD4 T cell differentiation and suscptibility of autoimmunity.” 2015. Doctoral Dissertation, Université Toulouse III – Paul Sabatier. Accessed April 15, 2021. http://www.theses.fr/2015TOU30284.

MLA Handbook (7^th Edition):

Stienne, Caroline. “Rôle du facteur de transcription Foxo3 dans la différenciation des LT CD4+ et la susceptibilité à l'auto-immunité : Foxo3 controls CD4 T cell differentiation and suscptibility of autoimmunity.” 2015. Web. 15 Apr 2021.

Vancouver:

Stienne C. Rôle du facteur de transcription Foxo3 dans la différenciation des LT CD4+ et la susceptibilité à l'auto-immunité : Foxo3 controls CD4 T cell differentiation and suscptibility of autoimmunity. [Internet] [Doctoral dissertation]. Université Toulouse III – Paul Sabatier; 2015. [cited 2021 Apr 15]. Available from: http://www.theses.fr/2015TOU30284.

Council of Science Editors:

Stienne C. Rôle du facteur de transcription Foxo3 dans la différenciation des LT CD4+ et la susceptibilité à l'auto-immunité : Foxo3 controls CD4 T cell differentiation and suscptibility of autoimmunity. [Doctoral Dissertation]. Université Toulouse III – Paul Sabatier; 2015. Available from: http://www.theses.fr/2015TOU30284

University of Rochester

16. Qi, Yilin (1980 - ). The Expression and Regulation of Amphiregulin in Human T Cells and Basophils.

Degree: PhD, 2012, University of Rochester

URL: http://hdl.handle.net/1802/25512

► Amphiregulin (AR), a member of the Epidermal Growth Factor family, is expressed during type 2 responses by activated mouse Th2 cells. AR produced by mouse… (more)

▼ Amphiregulin (AR), a member of the Epidermal Growth Factor family, is expressed during type 2 responses by activated mouse Th2 cells. AR produced by mouse hematopoietic cells contributes to the elimination of a nematode infection by a Type 2 effector response. We have now examined the regulation of expression of AR by human peripheral blood mononuclear cell T cells. Signaling through the TCR induced AR expression by human T cells, but in contrast to mouse cells, expression occurred in most or all T cell subsets, including naive and memory CD4 and CD8 T cells, Th1 and Th2 in vitro T cell lines, and subsets of memory CD4 T cells expressing several different chemokine receptors and cytokines. Strong stimuli, such as PMA and ionomycin, induced AR expression by a majority of naive and memory T cells. In addition of TCR stimulation, AR synthesis was enhanced by ligands that increased cAMP or directly activated PKA, a downstream component of the cAMP signaling pathway. Prostaglandin E2 and adenosine, natural ligands that bind to G protein coupled receptor and stimulate adenylyl cyclase activity, also enhanced AR synthesis while reducing synthesis of most other cytokines. Family of immune suppressive agents glucocorticoids, also showed opposite regulation of AR and cytokine expression. Thus AR synthesis by human T cells is regulated more by environmental signals than pre-commitment of T cells to a particular cytokine pattern. This may be appropriate for a cytokine more involved in repair than attack functions. Besides human T cells, we also observed a non-T cell population, which were basophils judged by morphology and lineage marker expression, expressing AR during human T cells activation. AR expression by basophils in response to anti-TCR stimulation required IL-3 produced by T cells, and IL-3 alone induced high levels of AR expression by purified basophils. These results suggest that the expression of AR in human immune cells also maintains a preference to type 2 immune responses through the production by basophils, which may contribute to tissue remodeling during type 2 immune responses such as asthma.

Subjects/Keywords: Amphiregulin; Human CD4 T Cell; Basophil; cAMP

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Qi, Y. (. -. ). (2012). The Expression and Regulation of Amphiregulin in Human T Cells and Basophils. (Doctoral Dissertation). University of Rochester. Retrieved from http://hdl.handle.net/1802/25512

Chicago Manual of Style (16^th Edition):

Qi, Yilin (1980 - ). “The Expression and Regulation of Amphiregulin in Human T Cells and Basophils.” 2012. Doctoral Dissertation, University of Rochester. Accessed April 15, 2021. http://hdl.handle.net/1802/25512.

MLA Handbook (7^th Edition):

Qi, Yilin (1980 - ). “The Expression and Regulation of Amphiregulin in Human T Cells and Basophils.” 2012. Web. 15 Apr 2021.

Vancouver:

Qi Y(-). The Expression and Regulation of Amphiregulin in Human T Cells and Basophils. [Internet] [Doctoral dissertation]. University of Rochester; 2012. [cited 2021 Apr 15]. Available from: http://hdl.handle.net/1802/25512.

Council of Science Editors:

Qi Y(-). The Expression and Regulation of Amphiregulin in Human T Cells and Basophils. [Doctoral Dissertation]. University of Rochester; 2012. Available from: http://hdl.handle.net/1802/25512

Universidad de Chile

17. Melgar Rodríguez, Samanta Azucena. Efecto de la estimulación con los distintos serotipos de Porphyromonas gingivalis y Aggregatibacter actinomycetemcomitans en la actividad de los linfocitos TCD4+ y la reabsorción ósea in vitro.

Degree: 2014, Universidad de Chile

URL: http://repositorio.uchile.cl/handle/2250/147391

► Las periodontitis son un conjunto de enfermedades de naturaleza inflamatoria y etiología infecciosa cuya causa es la biopelícula subgingival. Esta biopelícula está conformada por una… (more)

▼ Las periodontitis son un conjunto de enfermedades de naturaleza inflamatoria y etiología infecciosa cuya causa es la biopelícula subgingival. Esta biopelícula está conformada por una amplia variedad de bacterias Gram-negativas anaerobias, entre ellas, Porphyromonas gingivalis y Aggregatibacter actinomycetemcomitans. Sobre la base de la antigenicidad de la cápsula de P. gingivalis y del lipopolisacárido de A. actinomycetemcomitans se describen distintos serotipos bacterianos y se ha demostrado que entre estos distintos serotipos existe una potencialidad inmunogénica distinta en los linfocitos TCD4+. En particular, ante los serotipos K1 o K2 de P. gingivalis o el serotipo b de A. actinomycetemcomitans se describe un patrón de respuesta predominantemente tipo Th1 y Th17. En este estudio, linfocitos TCD4+ naïve humanos fueron activados por células dendríticas autólogas estimuladas con los serotipos K1-K6 de P. gingivalis o a-c de A. actinomycetemcomitans. Ante los serotipos K1 o K2 de P. gingivalis se detectaron mayores niveles de expresión de los factores de transcripción T-bet (Th1) y RORC2 (Th17), de secreción de RANKL y de diferenciación de osteoclastos TRAP+ en comparación a los otros serotipos bacterianos. Ante el serotipo b de A. actinomycetemcomitans se detectaron mayores niveles de expresión de T-bet y RORC2 y de secreción de RANKL en comparación a los serotipos a o c. Además, se analizó la frecuencia de proliferación de linfocitos TCD4+ de memoria obtenidos de pacientes con periodontitis y se detectó mayor respuesta ante los serotipos K1 o K2 de P. gingivalis o b de A. actinomycetemcomitans. Estos resultados confirman que los serotipos K1 o K2 de P. gingivalis o b de A. actinomycetemcomitans inducen un patrón de respuesta inmune predominantemente tipo Th1 (pro-inflamatorio) y Th17 (osteo-destructivo). Este patrón de respuesta Th1/Th17 se asoció a un incremento en la diferenciación de osteoclastos TRAP+ mediada por la producción de mayores niveles de RANKL. Finalmente, la mayor frecuencia de proliferación de linfocitos T de memoria ante los serotipos K1 o K2 de P. gingivalis o b de A. actinomycetemcomitans permite especular su participación durante la patogenia de la periodontitis, reflejada por la inducción de memoria inmunológica antígeno-específica. En conclusión, se demuestran diferencias en la respuesta de los linfocitos TCD4+ ante los distintos serotipos de P. gingivalis o A. actinomycetemcomitans y una mayor asociación de los serotipos K1 o K2 de P. gingivalis o b de A. actinomycetemcomitans a los fenómenos celulares y moleculares que explican la reabsorción ósea característica de las periodontitis.

Subjects/Keywords: Aggregatibacter actinomycetemcomitans; Linfocitos T CD4-Positivos

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Melgar Rodríguez, S. A. (2014). Efecto de la estimulación con los distintos serotipos de Porphyromonas gingivalis y Aggregatibacter actinomycetemcomitans en la actividad de los linfocitos TCD4+ y la reabsorción ósea in vitro. (Thesis). Universidad de Chile. Retrieved from http://repositorio.uchile.cl/handle/2250/147391

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Melgar Rodríguez, Samanta Azucena. “Efecto de la estimulación con los distintos serotipos de Porphyromonas gingivalis y Aggregatibacter actinomycetemcomitans en la actividad de los linfocitos TCD4+ y la reabsorción ósea in vitro.” 2014. Thesis, Universidad de Chile. Accessed April 15, 2021. http://repositorio.uchile.cl/handle/2250/147391.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Melgar Rodríguez, Samanta Azucena. “Efecto de la estimulación con los distintos serotipos de Porphyromonas gingivalis y Aggregatibacter actinomycetemcomitans en la actividad de los linfocitos TCD4+ y la reabsorción ósea in vitro.” 2014. Web. 15 Apr 2021.

Vancouver:

Melgar Rodríguez SA. Efecto de la estimulación con los distintos serotipos de Porphyromonas gingivalis y Aggregatibacter actinomycetemcomitans en la actividad de los linfocitos TCD4+ y la reabsorción ósea in vitro. [Internet] [Thesis]. Universidad de Chile; 2014. [cited 2021 Apr 15]. Available from: http://repositorio.uchile.cl/handle/2250/147391.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Melgar Rodríguez SA. Efecto de la estimulación con los distintos serotipos de Porphyromonas gingivalis y Aggregatibacter actinomycetemcomitans en la actividad de los linfocitos TCD4+ y la reabsorción ósea in vitro. [Thesis]. Universidad de Chile; 2014. Available from: http://repositorio.uchile.cl/handle/2250/147391

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

18. Laborel-Préneron, Emeline. Effets des sécrétomes de Staphylococcus aureus et Staphylococcus epidermidis du microbiote cutané d'enfants atopiques sur la réponse immunitaire T CD4 : Effects of staphylococcus aureus and staphylococcus epdidermidis secretomes from skin microbiota of atopic children on CD4T cell activation.

Degree: Docteur es, Immunologie, 2015, Université Toulouse III – Paul Sabatier

URL: http://www.theses.fr/2015TOU30093

►

La dermatite atopique (DA) est une maladie inflammatoire et prurigineuse de la peau, très fréquente chez les enfants et dont la prévalence augmente dans les… (more)

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La dermatite atopique (DA) est une maladie inflammatoire et prurigineuse de la peau, très fréquente chez les enfants et dont la prévalence augmente dans les pays industrialisés. La physiopathologie complexe de cette maladie met en jeu un défaut de la barrière cutanée et/ou des défauts génétiques résultant en une hypersensibilité aux allergènes de l'environnement tels que ceux issus d'acariens. Récemment, des études sur les interactions entre le système immunitaire et les bactéries commensales et pathogènes de la peau ont révélé leur importance dans cette maladie. Pour étudier le rôle du microbiote cutané dans la réponse T CD4+, des cohortes de jeunes enfants, atteints de DA et sensibilisés aux allergènes d'acariens (Der p) ou non DA (population contrôle), ont été recrutées. L'analyse du microbiote (MALDI-TOF) et du profil transcriptomique cutanés, ainsi que la quantification des T CD4+ anti-Derp (ELISpot) ont montré que la présence de S. aureus sur la peau inflammatoire des sujets AD était associée à des taux élevés d'IgE, des transcrits caractéristiques d'une orientation Th2/Th22 et à une réponse périphérique Th2. Des cellules dendritiques dérivées de monocytes (moDC) de donneurs sains produisent respectivement de l'IFN-gamma et de l'IL-10 en présence de sécrétomes issus de souches de S. aureus et S. epidermidis provenant de patients. La prolifération de lymphocytes T CD4+ stimulés avec des moDC allogéniques traitées avec le sécrétome de S. aureus est atténuée par le traitement simultané des moDC avec le sécrétome de S. epidermidis. Les sécrétomes de S. aureus sont capables d'inhiber directement l'activité suppressive de lymphocytes T régulateurs en l'absence de cellule présentatrice d'antigène. L'ensemble de nos résultats nous permet de penser que S. aureus est un facteur pro-inflammatoire de la DA en exacerbant la prolifération de lymphocytes Th2 résidents et en inhibant la fonction des lymphocytes T régulateurs. Favoriser les effets anti-inflammatoires des bactéries commensales telles que S. epidermidis liés à l'induction d'une sécrétion d'IL-10 par les cellules dendritiques de la peau pourrait bénéficier aux patients atteints de DA.

Atopic dermatitis (AD) is an inflammatory and pruritic skin disease frequently affecting children. Its prevalence is increasing in industrialized countries. Its complex pathophysiology involves a skin barrier dysfunction and/or genetic abnormalities leading to sensitivity to environmental allergens such as house dust mites. Interactions between the immune system and skin bacteria, pathogens and commensals, appeared to be important in the disease. To study the influence of skin microbiota in the CD4+ T cell response, we designed a cohort of young AD children sensitized to house dust mite allergens (Der p) and their counterparts (controls). Analysis of skin microbiota (MALDI-TOF), transcripts profiling and quantification of anti-Der p CD4+ T cells showed that the presence of S. aureus on inflamed skin of AD subjects was associated with high IgE levels, Th2/Th22 transcripts and…

Advisors/Committee Members: Davrinche, Christian (thesis director).

Subjects/Keywords: Microbiote cutané; Dermatite atopique; Réponse T CD4

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Laborel-Préneron, E. (2015). Effets des sécrétomes de Staphylococcus aureus et Staphylococcus epidermidis du microbiote cutané d'enfants atopiques sur la réponse immunitaire T CD4 : Effects of staphylococcus aureus and staphylococcus epdidermidis secretomes from skin microbiota of atopic children on CD4T cell activation. (Doctoral Dissertation). Université Toulouse III – Paul Sabatier. Retrieved from http://www.theses.fr/2015TOU30093

Chicago Manual of Style (16^th Edition):

Laborel-Préneron, Emeline. “Effets des sécrétomes de Staphylococcus aureus et Staphylococcus epidermidis du microbiote cutané d'enfants atopiques sur la réponse immunitaire T CD4 : Effects of staphylococcus aureus and staphylococcus epdidermidis secretomes from skin microbiota of atopic children on CD4T cell activation.” 2015. Doctoral Dissertation, Université Toulouse III – Paul Sabatier. Accessed April 15, 2021. http://www.theses.fr/2015TOU30093.

MLA Handbook (7^th Edition):

Laborel-Préneron, Emeline. “Effets des sécrétomes de Staphylococcus aureus et Staphylococcus epidermidis du microbiote cutané d'enfants atopiques sur la réponse immunitaire T CD4 : Effects of staphylococcus aureus and staphylococcus epdidermidis secretomes from skin microbiota of atopic children on CD4T cell activation.” 2015. Web. 15 Apr 2021.

Vancouver:

Laborel-Préneron E. Effets des sécrétomes de Staphylococcus aureus et Staphylococcus epidermidis du microbiote cutané d'enfants atopiques sur la réponse immunitaire T CD4 : Effects of staphylococcus aureus and staphylococcus epdidermidis secretomes from skin microbiota of atopic children on CD4T cell activation. [Internet] [Doctoral dissertation]. Université Toulouse III – Paul Sabatier; 2015. [cited 2021 Apr 15]. Available from: http://www.theses.fr/2015TOU30093.

Council of Science Editors:

Laborel-Préneron E. Effets des sécrétomes de Staphylococcus aureus et Staphylococcus epidermidis du microbiote cutané d'enfants atopiques sur la réponse immunitaire T CD4 : Effects of staphylococcus aureus and staphylococcus epdidermidis secretomes from skin microbiota of atopic children on CD4T cell activation. [Doctoral Dissertation]. Université Toulouse III – Paul Sabatier; 2015. Available from: http://www.theses.fr/2015TOU30093

19. Kassem, Sahar. Rôle du gène Vav1 et du probiotique Escherichia coli Nissle 1917 dans la susceptibilité à l'inflammation du système nerveux central : Role of the Vav1 gene and the probiotic Escherichia coli Nissle 1917 in the susceptibility to central nervous system inflammation.

Degree: Docteur es, Immunologie, 2015, Université Toulouse III – Paul Sabatier

URL: http://www.theses.fr/2015TOU30235

►

La Sclérose en Plaques (SEP) est une maladie d'origine multifactorielle qui se développe chez des individus génétiquement susceptibles en présence de facteurs environnementaux inducteurs. Ma… (more)

▼

La Sclérose en Plaques (SEP) est une maladie d'origine multifactorielle qui se développe chez des individus génétiquement susceptibles en présence de facteurs environnementaux inducteurs. Ma thèse avait pour objectif d'analyser les effets d'un facteur génétique, le variant R63W du gène Vav1 et d'un facteur environnemental, la souche "Escherichia coli Nissle 1917", sur le développement de l'encéphalomyélite auto-immune expérimentale (EAE), un modèle animal de la SEP. Une région de 1cM comportant un polymorphisme dans le gène Vav1 a en effet été identifiée au laboratoire comme étant responsable de la résistance des rats Brown-Norway à l'EAE. Afin d'établir formellement le rôle de ce polymorphisme dans ce modèle, une souris Knock-In Vav1R63W a été générée. Nous avons montré que les souris Vav1R63W développent une EAE moins sévère. Ceci est associé à un défaut de production de cytokines inflammatoires intrinsèque aux lymphocytes T (LT) CD4 qui n'est pas lié à une augmentation de la fréquence de LT régulateurs. Sur le plan moléculaire, Vav1R63W présente une activité adaptatrice défectueuse conduisant à la diminution de la phosphorylation de ERK, AKT et p38 mais à une activité enzymatique normale. Nos résultats montrent un rôle de la fonction adaptatrice de Vav1 dans les fonctions des LT CD4 et son implication dans la susceptibilité à l'inflammation du système nerveux central (SNC). L'analyse de l'effet d'un traitement oral par le probiotique E. coli Nissle 1917 (ECN) montre un effet bénéfique sur le développement de l'EAE. Ceci est associé à un défaut de la sécrétion de cytokines par les LT CD4, ainsi qu'à une diminution de l'infiltration de LT CD4 auto-réactifs dans le SNC. De plus, la barrière intestinale est moins altérée chez les souris traitées par ECN au cours du développement de l'EAE. L'effet bénéfique de ECN semble être dû à la production d'une génotoxine, la colibactine. Par contre, la colonisation néonatale des souris C57BL/6 par ECN ne reproduit pas le même effet observé à l'âge adulte. Dans l'ensemble, nos résultats montrent un effet bénéfique du changement de la fonction de Vav1 ainsi que du traitement par ECN sur le développement de l'EAE. L'analyse approfondie des mécanismes mis en jeu, permettra une meilleure compréhension de la pathogenèse de la SEP et pourrait contribuer à l'identification de nouvelles options thérapeutiques.

Multiple sclerosis (MS) is a demyelinating disease of the central nervous system. It develops in genetically susceptible individuals when they encounter specific environmental factors. The aim of my thesis was to analyze the role of a genetic factor (Vav1R63W variant) and an environmental factor (Escherichia coli Nissle 1917) in the development of experimental autoimmune encephalomyelitis (EAE), an animal model of MS. Previous genetic studies of my team suggest the implication of a polymorphism in the Vav1 gene in the resistance of Brown-Norway rats to EAE. In order to analyze the role of the identified polymorphism in the susceptibility to EAE, we generated a Knock-In mouse…

Advisors/Committee Members: Saoudi, Abdelhadi (thesis director), Colacios, Céline (thesis director).

Subjects/Keywords: Vav1; E.coli Nissle 1917; EAE; LT CD4

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Kassem, S. (2015). Rôle du gène Vav1 et du probiotique Escherichia coli Nissle 1917 dans la susceptibilité à l'inflammation du système nerveux central : Role of the Vav1 gene and the probiotic Escherichia coli Nissle 1917 in the susceptibility to central nervous system inflammation. (Doctoral Dissertation). Université Toulouse III – Paul Sabatier. Retrieved from http://www.theses.fr/2015TOU30235

Chicago Manual of Style (16^th Edition):

Kassem, Sahar. “Rôle du gène Vav1 et du probiotique Escherichia coli Nissle 1917 dans la susceptibilité à l'inflammation du système nerveux central : Role of the Vav1 gene and the probiotic Escherichia coli Nissle 1917 in the susceptibility to central nervous system inflammation.” 2015. Doctoral Dissertation, Université Toulouse III – Paul Sabatier. Accessed April 15, 2021. http://www.theses.fr/2015TOU30235.

MLA Handbook (7^th Edition):

Kassem, Sahar. “Rôle du gène Vav1 et du probiotique Escherichia coli Nissle 1917 dans la susceptibilité à l'inflammation du système nerveux central : Role of the Vav1 gene and the probiotic Escherichia coli Nissle 1917 in the susceptibility to central nervous system inflammation.” 2015. Web. 15 Apr 2021.

Vancouver:

Kassem S. Rôle du gène Vav1 et du probiotique Escherichia coli Nissle 1917 dans la susceptibilité à l'inflammation du système nerveux central : Role of the Vav1 gene and the probiotic Escherichia coli Nissle 1917 in the susceptibility to central nervous system inflammation. [Internet] [Doctoral dissertation]. Université Toulouse III – Paul Sabatier; 2015. [cited 2021 Apr 15]. Available from: http://www.theses.fr/2015TOU30235.

Council of Science Editors:

Kassem S. Rôle du gène Vav1 et du probiotique Escherichia coli Nissle 1917 dans la susceptibilité à l'inflammation du système nerveux central : Role of the Vav1 gene and the probiotic Escherichia coli Nissle 1917 in the susceptibility to central nervous system inflammation. [Doctoral Dissertation]. Université Toulouse III – Paul Sabatier; 2015. Available from: http://www.theses.fr/2015TOU30235

20. Bwalya, Marlon. Factors affecting CD4+T-lymphocyte count response to HAART in HIV/AIDS patients within 24 months of treatment at Chreso Ministries Art Centre.

Degree: 2011, University of Zimbabwe

URL: http://dspace.unza.zm/handle/123456789/557

► The general objective of this study was to identify factors that affect CD4-TLymphocyte count response in patients commenced on HAART within 24 months of treatment… (more)

▼ The general objective of this study was to identify factors that affect CD4-TLymphocyte count response in patients commenced on HAART within 24 months of treatment at Chreso Ministries VCT and ART centres. The elements of this study were files of clients of all age groups on HAART above 5 years of age who had at least four consecutive repeat CD4 count rechecks within 24months of treatment with all other necessary information of variables required for this study captured in smartcare at treatment initiation. According to May 2009 statistical report, Chreso Ministries ART centre which happened to be a study site had 7000 HIV positive clients on care and 3900 clients on HAART. This study was a retrospective cohort design and had a sample size of 340 files of clients. The sampling frame generated from the study population was subjected to computerized random selection to come up with the sample size of 340 medical files. The study was purely quantitative and involved reviewing clients’ records that have been captured on the smartcare database on clients who have been on HAART for more than 24months. The extracted data was entered in Epidata using Epi Info and was exported to SPSS for analysis. The Chi-Square test at 5% with crosstabulation tables was used to determine associations between the identified variables and CD4-Lymphocyte count response to HAART and the logistic regression analysis was used to predict the probability of CD4 count response to HAART using the variables of this study. The study was completed in 3months following approval from the Ethics Committee of the University of Zambia. The statement of the problem was the observed poor CD4 count response to treatment in most of the clients commenced on HAART. The factors at hand involved the social demographic factors (age, sex, income, alcohol consumption and employment status) ART factors (Adherence and ART regimen) and immunological factor (CD4 count at treatment initiation). In this study it was found that gender, alcohol consumption, nadire and regimen affects CD4 count response to HAART. It was found that men, non alcohol consumers and those that start HAART with baseline CD4 count above 350 cell/µL experienced a good CD4 response to HAART. Additionally, those who commenced treatment on truvada and devoted themselves to 95% adherence also experienced a good CD4 count response to HAART. On the other hand, age, smoking and employment status did not affect CD4 count response to HAART.

Subjects/Keywords: HIV/AIDS – Treatment; CD4+T-lymphocyte Count

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Bwalya, M. (2011). Factors affecting CD4+T-lymphocyte count response to HAART in HIV/AIDS patients within 24 months of treatment at Chreso Ministries Art Centre. (Thesis). University of Zimbabwe. Retrieved from http://dspace.unza.zm/handle/123456789/557

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Bwalya, Marlon. “Factors affecting CD4+T-lymphocyte count response to HAART in HIV/AIDS patients within 24 months of treatment at Chreso Ministries Art Centre.” 2011. Thesis, University of Zimbabwe. Accessed April 15, 2021. http://dspace.unza.zm/handle/123456789/557.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Bwalya, Marlon. “Factors affecting CD4+T-lymphocyte count response to HAART in HIV/AIDS patients within 24 months of treatment at Chreso Ministries Art Centre.” 2011. Web. 15 Apr 2021.

Vancouver:

Bwalya M. Factors affecting CD4+T-lymphocyte count response to HAART in HIV/AIDS patients within 24 months of treatment at Chreso Ministries Art Centre. [Internet] [Thesis]. University of Zimbabwe; 2011. [cited 2021 Apr 15]. Available from: http://dspace.unza.zm/handle/123456789/557.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Bwalya M. Factors affecting CD4+T-lymphocyte count response to HAART in HIV/AIDS patients within 24 months of treatment at Chreso Ministries Art Centre. [Thesis]. University of Zimbabwe; 2011. Available from: http://dspace.unza.zm/handle/123456789/557

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Toronto

21. Xu, An Qi. Microbe and host-derived mechanisms of protection from autoimmune diabetes in non-obese diabetic mice.

Degree: 2018, University of Toronto

URL: http://hdl.handle.net/1807/97648

►

Autoimmune diabetes results from T cell-mediated destruction of insulin-producing pancreatic β cells in both humans and non-obese diabetic (NOD) mice. Our lab previously observed that… (more)

Subjects/Keywords: autoimmune; CD4; diabetes; islet; microbiota; 0982

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APA (6^th Edition):

Xu, A. Q. (2018). Microbe and host-derived mechanisms of protection from autoimmune diabetes in non-obese diabetic mice. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/97648

Chicago Manual of Style (16^th Edition):

Xu, An Qi. “Microbe and host-derived mechanisms of protection from autoimmune diabetes in non-obese diabetic mice.” 2018. Masters Thesis, University of Toronto. Accessed April 15, 2021. http://hdl.handle.net/1807/97648.

MLA Handbook (7^th Edition):

Xu, An Qi. “Microbe and host-derived mechanisms of protection from autoimmune diabetes in non-obese diabetic mice.” 2018. Web. 15 Apr 2021.

Vancouver:

Xu AQ. Microbe and host-derived mechanisms of protection from autoimmune diabetes in non-obese diabetic mice. [Internet] [Masters thesis]. University of Toronto; 2018. [cited 2021 Apr 15]. Available from: http://hdl.handle.net/1807/97648.

Council of Science Editors:

Xu AQ. Microbe and host-derived mechanisms of protection from autoimmune diabetes in non-obese diabetic mice. [Masters Thesis]. University of Toronto; 2018. Available from: http://hdl.handle.net/1807/97648

Deakin University

22. Pade, Corinna. Dissecting the early entry steps of HIV-1 infection.

Degree: 2016, Deakin University

URL: http://hdl.handle.net/10536/DRO/DU:30092598

► The research revealed that HIV is able to undergo reorganization processes, perhaps to prime for entry into the host cell. It appears that cellular proteins… (more)

Subjects/Keywords: HIV infection; cellular proteins; CD4 receptor engagement

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APA (6^th Edition):

Pade, C. (2016). Dissecting the early entry steps of HIV-1 infection. (Thesis). Deakin University. Retrieved from http://hdl.handle.net/10536/DRO/DU:30092598

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Pade, Corinna. “Dissecting the early entry steps of HIV-1 infection.” 2016. Thesis, Deakin University. Accessed April 15, 2021. http://hdl.handle.net/10536/DRO/DU:30092598.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Pade, Corinna. “Dissecting the early entry steps of HIV-1 infection.” 2016. Web. 15 Apr 2021.

Vancouver:

Pade C. Dissecting the early entry steps of HIV-1 infection. [Internet] [Thesis]. Deakin University; 2016. [cited 2021 Apr 15]. Available from: http://hdl.handle.net/10536/DRO/DU:30092598.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Pade C. Dissecting the early entry steps of HIV-1 infection. [Thesis]. Deakin University; 2016. Available from: http://hdl.handle.net/10536/DRO/DU:30092598

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Cambridge

23. Ali, Jason. CD4 T cell allorecognition pathways in acute and chronic allograft rejection.

Degree: PhD, 2015, University of Cambridge

URL: https://www.repository.cam.ac.uk/handle/1810/252879https://www.repository.cam.ac.uk/bitstream/1810/252879/1/PhD%20Thesis%20REVISIONS.docx ; https://www.repository.cam.ac.uk/bitstream/1810/252879/2/license.txt ; https://www.repository.cam.ac.uk/bitstream/1810/252879/3/license_rdf ; https://www.repository.cam.ac.uk/bitstream/1810/252879/5/Ali-2015-PhD.pdf.txt ; https://www.repository.cam.ac.uk/bitstream/1810/252879/6/Ali-2015-PhD.pdf.jpg

► Solid organ transplantation is now an established and effective treatment option for end-stage organ failure. Whilst early outcomes have improved significantly over recent decades, longer-term… (more)

▼ Solid organ transplantation is now an established and effective treatment option for end-stage organ failure. Whilst early outcomes have improved significantly over recent decades, longer-term outcomes have changed little. Despite advances in immunosuppression, most transplanted organs suffer an inevitable decline in function attributed to chronic rejection. It is evident that the alloimmune response remains incompletely characterised. Crucially, despite description several decades ago, the precise contribution that the direct (recognition of intact allogeneic MHC) and indirect (recognition of self-MHC restricted allopeptide) pathways make to allograft rejection remains incompletely understood. In this thesis, murine models of heterotopic cardiac transplantation have been utilised to analyse these pathways. The key findings of this work are as follows: 1) If able to evade NK cell killing, passenger donor CD4 T cells can make cognate, direct-pathway, interactions with recipient B cells. This interaction results in augmentation of all arms of the alloimmune response and acceleration of allograft rejection. 2) Direct-pathway CD4 T cell allorecognition is restricted to the immediate post transplantation period. Donor APCs are the major source of MHC class II for direct-pathway priming, and these are cleared rapidly by both innate and adaptive responses of the recipient, effectively limiting the longevity of direct allorecognition. 3) The duration of indirect-pathway responses against different alloantigens is variable, limited by availability of donor antigen. Expression of donor MHC class II is restricted to APCs and possibly endothelium (where expression is transient) limiting the duration of indirect-pathway allorecognition against MHC class II alloantigen. Indirect-pathway CD4 T cell responses targeted against parenchymal alloantigen are long-lived, and can provide help for generating alloantibody against different MHC alloantigens. 4) In response to continual presentation of target epitope indirect-pathway CD4 T cell responses against parenchymal expressed alloantigen are long-lived. The continual division of these cells results in greatly increased numbers of alloantigen-specific CD4 T cells in the chronic phase of the response, but despite this, memory responses are impaired. 5) Generating indirect-pathway regulatory T cells specific for parenchymal expressed alloantigen appears to be the most effective strategy to ameliorating chronic rejection.

Subjects/Keywords: Allorecognition; Allograft; Rejection; CD4 T cell; Pathways

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APA (6^th Edition):

Ali, J. (2015). CD4 T cell allorecognition pathways in acute and chronic allograft rejection. (Doctoral Dissertation). University of Cambridge. Retrieved from https://www.repository.cam.ac.uk/handle/1810/252879https://www.repository.cam.ac.uk/bitstream/1810/252879/1/PhD%20Thesis%20REVISIONS.docx ; https://www.repository.cam.ac.uk/bitstream/1810/252879/2/license.txt ; https://www.repository.cam.ac.uk/bitstream/1810/252879/3/license_rdf ; https://www.repository.cam.ac.uk/bitstream/1810/252879/5/Ali-2015-PhD.pdf.txt ; https://www.repository.cam.ac.uk/bitstream/1810/252879/6/Ali-2015-PhD.pdf.jpg

Chicago Manual of Style (16^th Edition):

Ali, Jason. “CD4 T cell allorecognition pathways in acute and chronic allograft rejection.” 2015. Doctoral Dissertation, University of Cambridge. Accessed April 15, 2021. https://www.repository.cam.ac.uk/handle/1810/252879https://www.repository.cam.ac.uk/bitstream/1810/252879/1/PhD%20Thesis%20REVISIONS.docx ; https://www.repository.cam.ac.uk/bitstream/1810/252879/2/license.txt ; https://www.repository.cam.ac.uk/bitstream/1810/252879/3/license_rdf ; https://www.repository.cam.ac.uk/bitstream/1810/252879/5/Ali-2015-PhD.pdf.txt ; https://www.repository.cam.ac.uk/bitstream/1810/252879/6/Ali-2015-PhD.pdf.jpg.

MLA Handbook (7^th Edition):

Ali, Jason. “CD4 T cell allorecognition pathways in acute and chronic allograft rejection.” 2015. Web. 15 Apr 2021.

Vancouver:

Ali J. CD4 T cell allorecognition pathways in acute and chronic allograft rejection. [Internet] [Doctoral dissertation]. University of Cambridge; 2015. [cited 2021 Apr 15]. Available from: https://www.repository.cam.ac.uk/handle/1810/252879https://www.repository.cam.ac.uk/bitstream/1810/252879/1/PhD%20Thesis%20REVISIONS.docx ; https://www.repository.cam.ac.uk/bitstream/1810/252879/2/license.txt ; https://www.repository.cam.ac.uk/bitstream/1810/252879/3/license_rdf ; https://www.repository.cam.ac.uk/bitstream/1810/252879/5/Ali-2015-PhD.pdf.txt ; https://www.repository.cam.ac.uk/bitstream/1810/252879/6/Ali-2015-PhD.pdf.jpg.

Council of Science Editors:

Ali J. CD4 T cell allorecognition pathways in acute and chronic allograft rejection. [Doctoral Dissertation]. University of Cambridge; 2015. Available from: https://www.repository.cam.ac.uk/handle/1810/252879https://www.repository.cam.ac.uk/bitstream/1810/252879/1/PhD%20Thesis%20REVISIONS.docx ; https://www.repository.cam.ac.uk/bitstream/1810/252879/2/license.txt ; https://www.repository.cam.ac.uk/bitstream/1810/252879/3/license_rdf ; https://www.repository.cam.ac.uk/bitstream/1810/252879/5/Ali-2015-PhD.pdf.txt ; https://www.repository.cam.ac.uk/bitstream/1810/252879/6/Ali-2015-PhD.pdf.jpg

Boston University

24. Magohe, Albert Katana. Assessment of the effect of a protein calorie supplement on change in CD4 count among art-naïve female TB patients co-infected with HIV in Dar Es Salaam, Tanzania.

Degree: MS, Epidemiology, 2017, Boston University

URL: http://hdl.handle.net/2144/20864

► RATIONALE: Tuberculosis and HIV infection together form a highly mortal combination. Even after the advent of highly active antiretroviral therapy (HAART) medications, management for Tuberculosis… (more)

▼ RATIONALE: Tuberculosis and HIV infection together form a highly mortal combination. Even after the advent of highly active antiretroviral therapy (HAART) medications, management for Tuberculosis and HIV/AIDS still remains a challenge. Poor outcomes (in both morbidity and mortality) are still being witnessed throughout the world, and especially in the poorly developed countries that bear the bulk of the burden of the cases. It is assumed that one of the major contributors to the poor outcomes is poor nutritional status resulting from the disease process itself, poverty and toxicity from medications being used to treat these diseases that substantially reduce appetite. An assessment of the role that nutritional status has on change in CD4 as a surrogate marker of disease progression is therefore of importance. OBJECTIVES: To evaluate the role that nutritional supplementation has on change in CD4 in TB patients co-infected with HIV who are receiving standard care of treatment. METHODS: Data from a randomized controlled trial of a Protein Calorie Supplement (PCS) were used. To assess the effect of randomization to a nutritional supplement, baseline characteristics were compared among the intervention and the control groups and confounder variables, such as age, BMI, baseline CD4, socioeconomic status, previous exposure to TB and compliance with HAART medication were analyzed and adjusted for in a model using multivariate linear regression. RESULTS: 151 HIV-infected women with TB disease were enrolled; 72 received PCS while 79 did not. We found that the PCS intervention had no significant effect on change in CD4 between baseline and 8 months. Average change in CD4 count was similar for intervention and control groups (204 vs. 207 units). This similarity persisted after adjusting for baseline BMI and previous TB disease. CONCLUSION: Randomization (i.e. nutritional supplement) did not have a significant effect on change in CD4 count among study participants. However, an effect could have been masked by high compliance with ART.

Subjects/Keywords: Medicine; ART; CD4; HIV; Macronutrient; Tuberculosis

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APA (6^th Edition):

Magohe, A. K. (2017). Assessment of the effect of a protein calorie supplement on change in CD4 count among art-naïve female TB patients co-infected with HIV in Dar Es Salaam, Tanzania. (Masters Thesis). Boston University. Retrieved from http://hdl.handle.net/2144/20864

Chicago Manual of Style (16^th Edition):

Magohe, Albert Katana. “Assessment of the effect of a protein calorie supplement on change in CD4 count among art-naïve female TB patients co-infected with HIV in Dar Es Salaam, Tanzania.” 2017. Masters Thesis, Boston University. Accessed April 15, 2021. http://hdl.handle.net/2144/20864.

MLA Handbook (7^th Edition):

Magohe, Albert Katana. “Assessment of the effect of a protein calorie supplement on change in CD4 count among art-naïve female TB patients co-infected with HIV in Dar Es Salaam, Tanzania.” 2017. Web. 15 Apr 2021.

Vancouver:

Magohe AK. Assessment of the effect of a protein calorie supplement on change in CD4 count among art-naïve female TB patients co-infected with HIV in Dar Es Salaam, Tanzania. [Internet] [Masters thesis]. Boston University; 2017. [cited 2021 Apr 15]. Available from: http://hdl.handle.net/2144/20864.

Council of Science Editors:

Magohe AK. Assessment of the effect of a protein calorie supplement on change in CD4 count among art-naïve female TB patients co-infected with HIV in Dar Es Salaam, Tanzania. [Masters Thesis]. Boston University; 2017. Available from: http://hdl.handle.net/2144/20864

University of Washington

25. Moguche, Albanus O. Maintenance and function of antigen-specific CD4 T cells within the lung during tuberculosis.

Degree: PhD, 2014, University of Washington

URL: http://hdl.handle.net/1773/26105

► Tuberculosis (TB) is a chronic pulmonary disease caused by the intracellular bacterium Mycobacterium tuberculosis (Mtb). Even though CD4 T cells are critical for containing Mtb,… (more)

▼ Tuberculosis (TB) is a chronic pulmonary disease caused by the intracellular bacterium Mycobacterium tuberculosis (Mtb). Even though CD4 T cells are critical for containing Mtb, the immune system rarely eradicates the bacteria, necessitating the maintaining of an antigen-specific CD4 T cell response throughout the course of infection. How this response is maintained is not currently well understood. Here we show that in a murine model of TB, Mtb-specific CD4 T cells are subjected to chronic antigenic stimulation. Despite this chronic antigenic stimulation, a subset of these Mtb-specific CD4 T cells expressing the inhibitory receptor PD-1 exhibits hallmarks of memory T cells and their maintenance requires intrinsic expression of ICOS, the transcription factor Bcl6, and the chemokine receptor CXCR5. Furthermore we find that a majority of KLRG1+ IFN-γ producing CD4 T cells are located in the lung-associated vasculature and not in the lung parenchyma as previously thought. However, the PD-1+ population that shares features with follicular helper (Tfh) and memory T cells is principally located within the lung parenchyma. This distribution can be largely explained by considering the TB granuloma as a tertiary lymphoid structure that forms within the Mtb infected lung parenchyma. Contrary to previous reports, we found naïve CD44low CD4 T cells are excluded from lung parenchyma of uninfected mice but migrate into the lungs of Mtb-infected mice in a CCR7 dependent manner. PD-1+ Mtb-specific CD4 T cells express high levels of CD69 but have low levels of sphingosine-1-phosphate receptor 1 (S1PR1) and the transcription factor KLF2. In contrast, terminally differentiated KLRG1+ type 1 helper T cells (Th1) cells exhibit elevated expression of S1PR1 and KLF2, but are CD69low. These expression profiles likely explain the differential localization of these Mtb-specific cell populations and suggest that when effector Th1 cells are generated within the granuloma or draining lymph nodes, they egress into the blood in an S1P1R mediated manner. Our results help explain why the frequency of Th1 cells circulating in the blood does not correlate with immune protection, and provides a framework for understanding how immunity against TB is shaped by CD4 T cell trafficking into and out of granulomas. Finally, we found that CD4 T cells recognizing Mtb antigens expressed throughout infection have a reduced capacity to produce protective cytokines and are restricted in their ability to control Mtb due to persistent stimulation by antigen. Conversely, CD4 T cells that recognize different Mtb antigens whose expression wanes with chronic infection have a limited capacity to mediate protection because of suboptimal stimulation by cognate antigen. Collectively, these studies expand our understanding of the mechanisms that promote the maintenance and function of antigen-specific CD4 T cells in the lung during TB. The insights gained should aid in the rational design of new vaccines, not only against TB, but also against other chronic disease conditions… Advisors/Committee Members: Urdahl, Kevin B (advisor).

Subjects/Keywords: CD4 T cells; Immunology; Tuberculosis; Immunology; immunology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Moguche, A. O. (2014). Maintenance and function of antigen-specific CD4 T cells within the lung during tuberculosis. (Doctoral Dissertation). University of Washington. Retrieved from http://hdl.handle.net/1773/26105

Chicago Manual of Style (16^th Edition):

Moguche, Albanus O. “Maintenance and function of antigen-specific CD4 T cells within the lung during tuberculosis.” 2014. Doctoral Dissertation, University of Washington. Accessed April 15, 2021. http://hdl.handle.net/1773/26105.

MLA Handbook (7^th Edition):

Moguche, Albanus O. “Maintenance and function of antigen-specific CD4 T cells within the lung during tuberculosis.” 2014. Web. 15 Apr 2021.

Vancouver:

Moguche AO. Maintenance and function of antigen-specific CD4 T cells within the lung during tuberculosis. [Internet] [Doctoral dissertation]. University of Washington; 2014. [cited 2021 Apr 15]. Available from: http://hdl.handle.net/1773/26105.

Council of Science Editors:

Moguche AO. Maintenance and function of antigen-specific CD4 T cells within the lung during tuberculosis. [Doctoral Dissertation]. University of Washington; 2014. Available from: http://hdl.handle.net/1773/26105

University of Minnesota

26. Cabrera-Perez, Javier. Examining Helper T-cell Recovery After Sepsis.

Degree: PhD, Microbiology, Immunology and Cancer Biology, 2015, University of Minnesota

URL: http://hdl.handle.net/11299/185621

► Sepsis strikes 750,000 Americans every year with ~ 210,000 of these patients dying – far more than the number of deaths from prostate cancer, breast… (more)

Subjects/Keywords: CD4; infection; lymphopenia; sepsis; T-CELL; tetramer

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Cabrera-Perez, J. (2015). Examining Helper T-cell Recovery After Sepsis. (Doctoral Dissertation). University of Minnesota. Retrieved from http://hdl.handle.net/11299/185621

Chicago Manual of Style (16^th Edition):

Cabrera-Perez, Javier. “Examining Helper T-cell Recovery After Sepsis.” 2015. Doctoral Dissertation, University of Minnesota. Accessed April 15, 2021. http://hdl.handle.net/11299/185621.

MLA Handbook (7^th Edition):

Cabrera-Perez, Javier. “Examining Helper T-cell Recovery After Sepsis.” 2015. Web. 15 Apr 2021.

Vancouver:

Cabrera-Perez J. Examining Helper T-cell Recovery After Sepsis. [Internet] [Doctoral dissertation]. University of Minnesota; 2015. [cited 2021 Apr 15]. Available from: http://hdl.handle.net/11299/185621.

Council of Science Editors:

Cabrera-Perez J. Examining Helper T-cell Recovery After Sepsis. [Doctoral Dissertation]. University of Minnesota; 2015. Available from: http://hdl.handle.net/11299/185621

University of Minnesota

27. O'Donnell, Hope. Eliciting Th1 effector functions: A mechanism and role for innate amplification of the Th1 response during infection.

Degree: Microbiology, Immunology and Cancer Biology, 2014, University of Minnesota

URL: http://hdl.handle.net/11299/165052

► Innate and adaptive immunity have classically been considered as two distinct categories of cells and responses. Recently, however, an increasing appreciation for the dynamic interactions… (more)

▼ Innate and adaptive immunity have classically been considered as two distinct categories of cells and responses. Recently, however, an increasing appreciation for the dynamic interactions between these responses has developed. In this dissertation, this overlap is explored in the context of Th1 CD4 T cell production of IFN-γ (interferon-gamma) in response to innate stimuli. In particular, we first asked what triggers innate stimulation of Th1 cells, examining multiple ligands, infections and time points to show that this response occurred within broad contexts of intracellular infection. We then asked how T cells are able to recognize innate stimuli, focusing on whether the T cell intrinsic response relied upon direct LPS (lipopolysaccharide) recognition or indirect recognition of secondary signals. T cell intrinsic requirements were examined in mixed bone marrow chimeras that allowed T cells to be compared within the same environment. Upon demonstrating that the innate Th1 cell response required IL-18 (interleukin-18) receptor signaling, we next explored how T cell extrinsic PRRs (pattern recognition receptors) elicit effector functions through IL-18 secretion. Here, we showed a dual requirement for both TLR4 (toll-like receptor 4) and inflammasome pathways after LPS stimulation during Salmonella infection. The convergence of these pathways was required for increased IL-18 secretion, suggesting a dual level of control in production of such a proinflammatory cytokine. Finally, we asked whether the innate stimulation of Th1 cells is a required response pathway during clearance of Salmonella. Using Lck-cre x MyD88-loxP crossed mice, we demonstrated a deficiency in bacterial clearance in the absence of the signaling molecule MyD88 within T cells, which impairs the ability of Th1 cells to respond to IL-18, but not classical antigen stimulation. Together, this data suggests that the Th1 cell response utilizes a pathway of innate stimulation to amplify IFN-γ production under situations of severe inflammation, in which the classical adaptive response pathway may not be sufficient to mediate a strong and rapid response. Future work may explore additional infectious contexts, other CD4 T cell subsets, memory responses, and circumstances of immunopathology.

Subjects/Keywords: CD4; Chlamydia; Innate; LPS; Salmonella; Th1

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APA (6^th Edition):

O'Donnell, H. (2014). Eliciting Th1 effector functions: A mechanism and role for innate amplification of the Th1 response during infection. (Thesis). University of Minnesota. Retrieved from http://hdl.handle.net/11299/165052

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

O'Donnell, Hope. “Eliciting Th1 effector functions: A mechanism and role for innate amplification of the Th1 response during infection.” 2014. Thesis, University of Minnesota. Accessed April 15, 2021. http://hdl.handle.net/11299/165052.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

O'Donnell, Hope. “Eliciting Th1 effector functions: A mechanism and role for innate amplification of the Th1 response during infection.” 2014. Web. 15 Apr 2021.

Vancouver:

O'Donnell H. Eliciting Th1 effector functions: A mechanism and role for innate amplification of the Th1 response during infection. [Internet] [Thesis]. University of Minnesota; 2014. [cited 2021 Apr 15]. Available from: http://hdl.handle.net/11299/165052.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

O'Donnell H. Eliciting Th1 effector functions: A mechanism and role for innate amplification of the Th1 response during infection. [Thesis]. University of Minnesota; 2014. Available from: http://hdl.handle.net/11299/165052

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Minnesota

28. Kotov, Jessica. CD4+ T cell differentiation and help to B cells.

Degree: PhD, Microbiology, Immunology and Cancer Biology, 2019, University of Minnesota

URL: http://hdl.handle.net/11299/202414

► Vaccines save 2.5 million lives per year. Vaccine efficacy is largely dependent on the successful generation of antibodies by B cells for the elimination of… (more)

▼ Vaccines save 2.5 million lives per year. Vaccine efficacy is largely dependent on the successful generation of antibodies by B cells for the elimination of pathogens like the influenza virus. T follicular helper (Tfh) cells are a type of CD4+ T cell that provides critical help to B cells for this process. My thesis research involves studying factors that promote Tfh cell formation and therefore B cell responses. This research is significant because it will provide better understanding of how Tfh cells are generated, which can be implemented during vaccine design. Using an approach to track both polyclonal antigen- specific CD4+ T and B cells within the same mouse after Complete Freund’s Adjuvant immunization, we found that the expression of BCOR protein in CD4+ T cells was critical for optimal Tfh formation. Reduced Tfh development as a result of BCOR absence also led to reduced germinal center B cell and antibody-secreting plasma cell formation. Thus, BCOR plays a critical role in promoting Tfh differentiation and B cell responses. The role of BCOR in CD4+ T cell differentiation was also examined after infection of mice with the extracellular pathogen Streptococcus pyogenes (Group A Streptococcus). In this context, BCOR enhanced the development of another CD4+ T cell type called T helper 17 (Th17) cells. Th17 cells promote protection by secreting cytokines, like IL-17A, that drive trafficking of neutrophils to the site of infection to kill bacteria. Identifying the drivers of Th17 cells will inform the development of a Th17- focused Streptococcus pyogenes vaccine for humans, which is currently unavailable. Because the efficacy of most vaccines is based on the process by which CD4+ T cells stimulate antibody responses, we wanted to better understand the role of different CD4+ T cell types on the B cell response. Tfh cells, in addition to Th1 and Th17 cells, were found to contribute to the production of early antibody-secreting B cells. This work provides insight into how non-Tfh cells also contribute to the B cell response, which is understudied in the field of B cell biology. Better understanding the process of CD4+ T cell help for generating antibody-secreting B cells is critical for producing efficacious vaccines.

Subjects/Keywords: B; BCOR; CD4; help; tfh; th17

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Kotov, J. (2019). CD4+ T cell differentiation and help to B cells. (Doctoral Dissertation). University of Minnesota. Retrieved from http://hdl.handle.net/11299/202414

Chicago Manual of Style (16^th Edition):

Kotov, Jessica. “CD4+ T cell differentiation and help to B cells.” 2019. Doctoral Dissertation, University of Minnesota. Accessed April 15, 2021. http://hdl.handle.net/11299/202414.

MLA Handbook (7^th Edition):

Kotov, Jessica. “CD4+ T cell differentiation and help to B cells.” 2019. Web. 15 Apr 2021.

Vancouver:

Kotov J. CD4+ T cell differentiation and help to B cells. [Internet] [Doctoral dissertation]. University of Minnesota; 2019. [cited 2021 Apr 15]. Available from: http://hdl.handle.net/11299/202414.

Council of Science Editors:

Kotov J. CD4+ T cell differentiation and help to B cells. [Doctoral Dissertation]. University of Minnesota; 2019. Available from: http://hdl.handle.net/11299/202414

University of Arizona

29. Bronnimann, Heather. Functional Analysis of Interactions within the TCR-CD3-pMHC-CD4 Macro-complex .

Degree: 2016, University of Arizona

URL: http://hdl.handle.net/10150/612427

► CD4⁺ T cells are a critical component of the adaptive immune compartment. Each T cell expresses a clonotypic T cell receptor (TCR) that must discriminate… (more)

▼ CD4⁺ T cells are a critical component of the adaptive immune compartment. Each T cell expresses a clonotypic T cell receptor (TCR) that must discriminate between self and foreign peptides presented in major histocompatibility molecules (pMHC) on the surface of antigen presenting cells to direct T cell fate decisions. Information regarding TCR-pMHC interactions must then be transmitted to the TCR-associated CD3 signaling modules, which contain ITAMs that serve as signaling substrates for Src kinases. The Src kinase, Lck, is recruited to the pMHC-bound TCR-CD3 complex via association with the CD4 coreceptor that binds MHCII. It is therefore through the coordinated interactions within the TCR-CD3-pMHC-CD4 macro-complex that productive TCR signaling can occur to inform T cell activation and fate decisions. While much is known regarding the structure of the individual subunits that make up the TCR-CD3-pMHC-CD4 macro-complex, there is little information regarding how these components come together to initiate TCR signaling and determine functional outcomes. Here, we have interrogated how interaction of these individual components leads to productive T cell activation. Specifically, we interrogated the nature of TCR-MHC interactions and provide evidence that there is intrinsic specificity of the TCR for MHCII. We have also built mouse models to determine the role of TCR-CD3 interactions and TCR dimerization in the transmission of information from the TCR to the CD3 subunits following TCR-pMHC engagement. Finally, we show that both the CD4 transmembrane and extracellular domains contribute to T cell activation in vitro. Overall, this work provides insight into how the constituents of the TCR-CD3-pMHC-CD4 macro-complex interact to initiate T cell fate and function. Advisors/Committee Members: Kuhns, Michael (advisor), Frelinger, Jeffrey (committeemember), Lybarger, Lonnie (committeemember), So, Magdalene (committeemember), Campos, Samuel (committeemember), Kuhns, Michael (committeemember).

Subjects/Keywords: pMHC; restriction; T cell; TCR; Immunobiology; CD4

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Bronnimann, H. (2016). Functional Analysis of Interactions within the TCR-CD3-pMHC-CD4 Macro-complex . (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/612427

Chicago Manual of Style (16^th Edition):

Bronnimann, Heather. “Functional Analysis of Interactions within the TCR-CD3-pMHC-CD4 Macro-complex .” 2016. Doctoral Dissertation, University of Arizona. Accessed April 15, 2021. http://hdl.handle.net/10150/612427.

MLA Handbook (7^th Edition):

Bronnimann, Heather. “Functional Analysis of Interactions within the TCR-CD3-pMHC-CD4 Macro-complex .” 2016. Web. 15 Apr 2021.

Vancouver:

Bronnimann H. Functional Analysis of Interactions within the TCR-CD3-pMHC-CD4 Macro-complex . [Internet] [Doctoral dissertation]. University of Arizona; 2016. [cited 2021 Apr 15]. Available from: http://hdl.handle.net/10150/612427.

Council of Science Editors:

Bronnimann H. Functional Analysis of Interactions within the TCR-CD3-pMHC-CD4 Macro-complex . [Doctoral Dissertation]. University of Arizona; 2016. Available from: http://hdl.handle.net/10150/612427

Virginia Tech

30. Carbo Barrios, Adria. Transdisciplinary Strategies to Study the Mechanisms of CD4+ T cell Differentiation and Heterogeneity.

Degree: PhD, Genetics, Bioinformatics, and Computational Biology, 2014, Virginia Tech

URL: http://hdl.handle.net/10919/64833

► CD4+ T cells mediate and orchestrate a tremendous panoply of lymphoid cell subsets in the human immune system. CD4+ T cells are able to differentiate… (more)

▼ CD4+ T cells mediate and orchestrate a tremendous panoply of lymphoid cell subsets in the human immune system. CD4+ T cells are able to differentiate into either effector pro-inflammatory or regulatory anti-inflammatory subsets depending on the cytokine milieu in their environment. This complex process is mediated through a variety of cytokines and soluble factors. Yet, the mechanisms of action underlying the process of differentiation and plasticity of this interesting immune subset are incompletely understood. To gain a better understanding of the CD4+ T cell differentiation and function, here we present an array of different strategies to model and validate CD4+ T cell differentiation and heterogeneity. The approaches presented here vary from ordinary-differential equation-based to agent-based simulations, from data-driven to theory-based approaches, and from intracellular mathematical to tissue-level or cellular modeling. The knowledge generated throughout this dissertation exemplifies how a combination of computational modeling with experimental immunology can efficiently advance the scene on CD4+ T cell differentiation. In this thesis I present i) an overview on CD4+ T cell differentiation and an introduction to which computational strategies have been adopted in the field to tackle with this problem, ii) ODE-based modeling and predictions on Th17 plasticity modulated by PPARγ, iii) ODE- and ABM-based cellular level modeling of immune responses towards Helicobacter pylori and the role of CD4+ T cell subsets on it, iv) Intracellular strategies to validate a potential therapeutic target within a CD4+ T cell to treat H. pylori infection, and finally v) data-driven strategies to model Th17 differentiation based on sequencing or microarray data to generate novel predictions on specific components. I present both mathematical and computational work as well as experimental work, in vitro and in vivo with animal models, to demonstrate how computational immunology and immunoinformatics can help, not only in understanding this complex process, but also in the development of immune therapeutics for infectious, allergic and immune-mediated diseases. Advisors/Committee Members: Bassaganya-Riera, Josep (committeechair), Hoops, Stefan (committee member), Bevan, David R. (committee member), Hontecillas-Magarzo, Raquel (committee member).

Subjects/Keywords: Immunology; CD4+ T cells; computational modeling

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Carbo Barrios, A. (2014). Transdisciplinary Strategies to Study the Mechanisms of CD4+ T cell Differentiation and Heterogeneity. (Doctoral Dissertation). Virginia Tech. Retrieved from http://hdl.handle.net/10919/64833

Chicago Manual of Style (16^th Edition):

Carbo Barrios, Adria. “Transdisciplinary Strategies to Study the Mechanisms of CD4+ T cell Differentiation and Heterogeneity.” 2014. Doctoral Dissertation, Virginia Tech. Accessed April 15, 2021. http://hdl.handle.net/10919/64833.

MLA Handbook (7^th Edition):

Carbo Barrios, Adria. “Transdisciplinary Strategies to Study the Mechanisms of CD4+ T cell Differentiation and Heterogeneity.” 2014. Web. 15 Apr 2021.

Vancouver:

Carbo Barrios A. Transdisciplinary Strategies to Study the Mechanisms of CD4+ T cell Differentiation and Heterogeneity. [Internet] [Doctoral dissertation]. Virginia Tech; 2014. [cited 2021 Apr 15]. Available from: http://hdl.handle.net/10919/64833.

Council of Science Editors:

Carbo Barrios A. Transdisciplinary Strategies to Study the Mechanisms of CD4+ T cell Differentiation and Heterogeneity. [Doctoral Dissertation]. Virginia Tech; 2014. Available from: http://hdl.handle.net/10919/64833

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Open Access Theses and Dissertations