subject:(T cells)

1. Belmont, Judson. Technologies for Phosphoproteomic Interrogation of T Cell Signaling.

Degree: Department of Molecular Biology, Cell Biology and Biochemistry, 2017, Brown University

URL: https://repository.library.brown.edu/studio/item/bdr:792636/

► The ability to detect and adapt to changing conditions and circumstances is a requirement of life at both the organismal and cellular levels. Inside the… (more)

▼ The ability to detect and adapt to changing conditions and circumstances is a requirement of life at both the organismal and cellular levels. Inside the cell, rapid and fine-tuned responses to environmental cues can be achieved through dynamic post-translational modifications (PTMs) of proteins. Significant insights into the activity and dependencies of signaling pathways can therefore be gleaned from global surveys of PTM events, and in particular protein phosphorylation, as it is absolutely essential in the signaling cascades mediating the downstream functions of receptor tyrosine kinase systems. In T cells, coordinated phosphorylation of tyrosine residues is critical for transmission of signals from the activated T cell receptor. Investigations into the dynamic phosphoproteome of T cells have been greatly assisted by advances in mass spectrometry, which allows for the identification and quantitation of thousands of PTMs simultaneously without a requirement for site-specific antibodies. However, despite the increasing resolution and decreasing cost of mass spectrometry assays, the complex network of phosphorylation events governing T cell activation has been only incompletely characterized. In particular, while it is now appreciated that numerous feedback pathways within the T cell phosphoproteome work together to regulate the initiation of immune responses, when and where feedback loops occur in the pathway is poorly understood. To better understand the role that critical T cell signaling components play in feedback regulation of the T cell receptor pathway, we conducted a phosphoproteomic study into the role of Phospholipase C-γ1 in mediating the activation state of the receptor-proximal signaling machinery. Additionally, we investigated the application of optimized chromatography configurations to T cell phosphoproteomics, and demonstrated the immense potential to achieve greater qualitative and quantitative insights into the T cell signaling machinery. Finally, to support the visualization, management, annotation, and analysis of this proteomic data, we designed and implemented new tools to expedite discoveries from large LC-MS datasets. The subject of this work is therefore the insights we have gained into the mechanisms governing T cell activation and regulation as well as the technical and technological innovations that made those insights possible. Advisors/Committee Members: Salomon, Art (Advisor), Gruppuso, Philip (Reader), de Graffenreid, Christopher (Reader), Neretti, Nicola (Reader), Gerber, Scott (Reader).

Subjects/Keywords: T cells

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APA (6^th Edition):

Belmont, J. (2017). Technologies for Phosphoproteomic Interrogation of T Cell Signaling. (Thesis). Brown University. Retrieved from https://repository.library.brown.edu/studio/item/bdr:792636/

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):

Belmont, Judson. “Technologies for Phosphoproteomic Interrogation of T Cell Signaling.” 2017. Thesis, Brown University. Accessed February 17, 2020. https://repository.library.brown.edu/studio/item/bdr:792636/.

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

MLA Handbook (7^th Edition):

Belmont, Judson. “Technologies for Phosphoproteomic Interrogation of T Cell Signaling.” 2017. Web. 17 Feb 2020.

Vancouver:

Belmont J. Technologies for Phosphoproteomic Interrogation of T Cell Signaling. [Internet] [Thesis]. Brown University; 2017. [cited 2020 Feb 17]. Available from: https://repository.library.brown.edu/studio/item/bdr:792636/.

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

Council of Science Editors:

Belmont J. Technologies for Phosphoproteomic Interrogation of T Cell Signaling. [Thesis]. Brown University; 2017. Available from: https://repository.library.brown.edu/studio/item/bdr:792636/

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

University of Oxford

2. Kurioka, Ayako. Mucosal associated invariant T cells and CD161 expressing natural killer cells.

Degree: PhD, 2015, University of Oxford

URL: https://ora.ox.ac.uk/objects/uuid:f994e661-d241-4a1c-ac56-b6bea73346ac ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.730591

► Mucosal-associated invariant T (MAIT) cells are a population of innate-like lymphocytes within the gut, liver and blood, expressing a semi-invariant T cell receptor (TCR) and… (more)

Subjects/Keywords: T cells

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APA (6^th Edition):

Kurioka, A. (2015). Mucosal associated invariant T cells and CD161 expressing natural killer cells. (Doctoral Dissertation). University of Oxford. Retrieved from https://ora.ox.ac.uk/objects/uuid:f994e661-d241-4a1c-ac56-b6bea73346ac ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.730591

Chicago Manual of Style (16^th Edition):

Kurioka, Ayako. “Mucosal associated invariant T cells and CD161 expressing natural killer cells.” 2015. Doctoral Dissertation, University of Oxford. Accessed February 17, 2020. https://ora.ox.ac.uk/objects/uuid:f994e661-d241-4a1c-ac56-b6bea73346ac ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.730591.

MLA Handbook (7^th Edition):

Kurioka, Ayako. “Mucosal associated invariant T cells and CD161 expressing natural killer cells.” 2015. Web. 17 Feb 2020.

Vancouver:

Kurioka A. Mucosal associated invariant T cells and CD161 expressing natural killer cells. [Internet] [Doctoral dissertation]. University of Oxford; 2015. [cited 2020 Feb 17]. Available from: https://ora.ox.ac.uk/objects/uuid:f994e661-d241-4a1c-ac56-b6bea73346ac ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.730591.

Council of Science Editors:

Kurioka A. Mucosal associated invariant T cells and CD161 expressing natural killer cells. [Doctoral Dissertation]. University of Oxford; 2015. Available from: https://ora.ox.ac.uk/objects/uuid:f994e661-d241-4a1c-ac56-b6bea73346ac ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.730591

University of Hong Kong

3. Zheng, Jian. Generation of human allo-antigen specific CD4+ and CD8+ regulatory T cells with CD40-activated B cells.

Degree: PhD, 2011, University of Hong Kong

URL: Zheng, J. [郑健]. (2011). Generation of human allo-antigen specific CD4+ and CD8+ regulatory T cells with CD40-activated B cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4692296 ; http://dx.doi.org/10.5353/th_b4692296 ; http://hdl.handle.net/10722/173971

published_or_final_version

Paediatrics and Adolescent Medicine

Doctoral

Doctor of Philosophy

Advisors/Committee Members: Tu, W, Lau, YL.

Subjects/Keywords: B cells.; T cells.

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APA (6^th Edition):

Zheng, J. (2011). Generation of human allo-antigen specific CD4+ and CD8+ regulatory T cells with CD40-activated B cells. (Doctoral Dissertation). University of Hong Kong. Retrieved from Zheng, J. [郑健]. (2011). Generation of human allo-antigen specific CD4+ and CD8+ regulatory T cells with CD40-activated B cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4692296 ; http://dx.doi.org/10.5353/th_b4692296 ; http://hdl.handle.net/10722/173971

Chicago Manual of Style (16^th Edition):

Zheng, Jian. “Generation of human allo-antigen specific CD4+ and CD8+ regulatory T cells with CD40-activated B cells.” 2011. Doctoral Dissertation, University of Hong Kong. Accessed February 17, 2020. Zheng, J. [郑健]. (2011). Generation of human allo-antigen specific CD4+ and CD8+ regulatory T cells with CD40-activated B cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4692296 ; http://dx.doi.org/10.5353/th_b4692296 ; http://hdl.handle.net/10722/173971.

MLA Handbook (7^th Edition):

Zheng, Jian. “Generation of human allo-antigen specific CD4+ and CD8+ regulatory T cells with CD40-activated B cells.” 2011. Web. 17 Feb 2020.

Vancouver:

Zheng J. Generation of human allo-antigen specific CD4+ and CD8+ regulatory T cells with CD40-activated B cells. [Internet] [Doctoral dissertation]. University of Hong Kong; 2011. [cited 2020 Feb 17]. Available from: Zheng, J. [郑健]. (2011). Generation of human allo-antigen specific CD4+ and CD8+ regulatory T cells with CD40-activated B cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4692296 ; http://dx.doi.org/10.5353/th_b4692296 ; http://hdl.handle.net/10722/173971.

Council of Science Editors:

Zheng J. Generation of human allo-antigen specific CD4+ and CD8+ regulatory T cells with CD40-activated B cells. [Doctoral Dissertation]. University of Hong Kong; 2011. Available from: Zheng, J. [郑健]. (2011). Generation of human allo-antigen specific CD4+ and CD8+ regulatory T cells with CD40-activated B cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4692296 ; http://dx.doi.org/10.5353/th_b4692296 ; http://hdl.handle.net/10722/173971

University of Hong Kong

4. Chan, Ping-lung. Roles of TLR5 and ICOS on the human allogenic CD40-activated B cell-induced CD4hiCD25+ regulatory T cells.

Degree: PhD, 2011, University of Hong Kong

URL: Chan, P. [陳秉隆]. (2011). Roles of TLR5 and ICOS on the human allogenic CD40-activated B cell-induced CD4hiCD25+ regulatory T cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4714973 ; http://dx.doi.org/10.5353/th_b4714973 ; http://hdl.handle.net/10722/145689

published_or_final_version

Paediatrics and Adolescent Medicine

Doctoral

Doctor of Philosophy

Advisors/Committee Members: Tu, W, Lau, YL.

Subjects/Keywords: CD antigens.; T cells.; T-cells - Receptors.

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APA (6^th Edition):

Chan, P. (2011). Roles of TLR5 and ICOS on the human allogenic CD40-activated B cell-induced CD4hiCD25+ regulatory T cells. (Doctoral Dissertation). University of Hong Kong. Retrieved from Chan, P. [陳秉隆]. (2011). Roles of TLR5 and ICOS on the human allogenic CD40-activated B cell-induced CD4hiCD25+ regulatory T cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4714973 ; http://dx.doi.org/10.5353/th_b4714973 ; http://hdl.handle.net/10722/145689

Chicago Manual of Style (16^th Edition):

Chan, Ping-lung. “Roles of TLR5 and ICOS on the human allogenic CD40-activated B cell-induced CD4hiCD25+ regulatory T cells.” 2011. Doctoral Dissertation, University of Hong Kong. Accessed February 17, 2020. Chan, P. [陳秉隆]. (2011). Roles of TLR5 and ICOS on the human allogenic CD40-activated B cell-induced CD4hiCD25+ regulatory T cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4714973 ; http://dx.doi.org/10.5353/th_b4714973 ; http://hdl.handle.net/10722/145689.

MLA Handbook (7^th Edition):

Chan, Ping-lung. “Roles of TLR5 and ICOS on the human allogenic CD40-activated B cell-induced CD4hiCD25+ regulatory T cells.” 2011. Web. 17 Feb 2020.

Vancouver:

Chan P. Roles of TLR5 and ICOS on the human allogenic CD40-activated B cell-induced CD4hiCD25+ regulatory T cells. [Internet] [Doctoral dissertation]. University of Hong Kong; 2011. [cited 2020 Feb 17]. Available from: Chan, P. [陳秉隆]. (2011). Roles of TLR5 and ICOS on the human allogenic CD40-activated B cell-induced CD4hiCD25+ regulatory T cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4714973 ; http://dx.doi.org/10.5353/th_b4714973 ; http://hdl.handle.net/10722/145689.

Council of Science Editors:

Chan P. Roles of TLR5 and ICOS on the human allogenic CD40-activated B cell-induced CD4hiCD25+ regulatory T cells. [Doctoral Dissertation]. University of Hong Kong; 2011. Available from: Chan, P. [陳秉隆]. (2011). Roles of TLR5 and ICOS on the human allogenic CD40-activated B cell-induced CD4hiCD25+ regulatory T cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4714973 ; http://dx.doi.org/10.5353/th_b4714973 ; http://hdl.handle.net/10722/145689

University of Georgia

5. Shane, Hillary Lee. Development of anti-viral CD8+ T cell memory in the respiratory environment.

Degree: PhD, Cellular Biology, 2014, University of Georgia

URL: http://purl.galileo.usg.edu/uga_etd/shane_hillary_l_201412_phd

► Mucosal surfaces represent the major portal by which pathogens enter the body, yet there is limited understanding of how CD8+ T cell responses develop and… (more)

▼ Mucosal surfaces represent the major portal by which pathogens enter the body, yet there is limited understanding of how CD8+ T cell responses develop and are maintained at these sites. The majority of knowledge on CD8+ T cell responses and memory formation has been amassed in models of acute, systemic infections, even though it is appreciated that mucosal sites consist of immunological environments unique from sites in which responses to systemic infections develop. Moreover, a firm understanding of how memory is generated in mucosal sites is important for the development of vaccines, which may employ a systemic or mucosal route of immunization, such as those directed against influenza virus. Vaccines that target protective CD8+ T cell responses are of particular interest for influenza, as memory CD8+ T cells can limit severe disease and can offer protection against multiple influenza subtypes. This study shows that the respiratory environment can directly influence CD8+ cell responses, resulting in localized changes in CD8+ T cell memory formation as well as broadly inhibiting the formation of long-lived memory cells. We show that the mucosal cytokine thymic stromal lymphopoietin (TSLP) is produced early following mucosal influenza infection, and acts on CD8+ effector cells in a direct and non-redundant way, promoting the proliferation of these cells at the site of infection. This early response influences memory development resulting in more of an effector memory population of cells. I go on to show that by comparing vesicular stomatitis virus infection delivered by the intranasal or intravenous route, that the respiratory environment results in memory CD8+ T cell population that is skewed from the archetypical memory developmental programs defined in systemic models of infection, resulting in numerically deficient memory. Together this work suggests that the respiratory environment can uniquely transform CD8+ T responses towards a more short-lived population of cells, and that protective vaccination strategy will require thoughtful modifications to bypass the restrictions conferred by the respiratory environment and promote memory development. Advisors/Committee Members: Kimberly Klonowski.

Subjects/Keywords: CD8+ T cells

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APA (6^th Edition):

Shane, H. L. (2014). Development of anti-viral CD8+ T cell memory in the respiratory environment. (Doctoral Dissertation). University of Georgia. Retrieved from http://purl.galileo.usg.edu/uga_etd/shane_hillary_l_201412_phd

Chicago Manual of Style (16^th Edition):

Shane, Hillary Lee. “Development of anti-viral CD8+ T cell memory in the respiratory environment.” 2014. Doctoral Dissertation, University of Georgia. Accessed February 17, 2020. http://purl.galileo.usg.edu/uga_etd/shane_hillary_l_201412_phd.

MLA Handbook (7^th Edition):

Shane, Hillary Lee. “Development of anti-viral CD8+ T cell memory in the respiratory environment.” 2014. Web. 17 Feb 2020.

Vancouver:

Shane HL. Development of anti-viral CD8+ T cell memory in the respiratory environment. [Internet] [Doctoral dissertation]. University of Georgia; 2014. [cited 2020 Feb 17]. Available from: http://purl.galileo.usg.edu/uga_etd/shane_hillary_l_201412_phd.

Council of Science Editors:

Shane HL. Development of anti-viral CD8+ T cell memory in the respiratory environment. [Doctoral Dissertation]. University of Georgia; 2014. Available from: http://purl.galileo.usg.edu/uga_etd/shane_hillary_l_201412_phd

6. Nevers, Tania A. Inflammatory and dysfunctional regulatory T cells in adverse pregnancy outcomes.

Degree: PhD, Pathobiology, 2012, Brown University

URL: https://repository.library.brown.edu/studio/item/bdr:297562/

► The etiologies for adverse pregnancy outcomes such as recurrent spontaneous abortion, preeclampsia, preterm birth and gestational diabetes mellitus (GDM) are multi-factorial and remain poorly understood.… (more)

▼ The etiologies for adverse pregnancy outcomes such as recurrent spontaneous abortion, preeclampsia, preterm birth and gestational diabetes mellitus (GDM) are multi-factorial and remain poorly understood. The main reasons for enigmatic state of adverse pregnancy outcomes can be assigned to lack of well defined animal models in response to inflammatory triggers and early pregnancy predictive assays and biomarkers. However, these pregnancy complications have a common contributor in inflammation at the maternal-fetal interface. In normal pregnancy, a state of immune tolerance is choreographed involving pro- and anti-inflammatory signals. Regulatory T cells (Tregs) have acquired a premier role in regulating immune tolerance systemically and at the maternal-fetal interface. Here we focus on Tregs for their phenotypic and functional dysregulation in mouse and human models of pregnancy complications. Importantly, we invoke the role of IL-10, a signature cytokine of Tregs, and human chorionic gonadotropin (hCG) in maintaining normal pregnancy. Our overarching hypothesis is that uterine regulatory T cells are dysfunctional in adverse pregnancies associated with infection and /or inflammation and may be normalized by IL-10 and hCG. This work explores dysregulation of uterine Tregs by utilizing mouse models of adverse pregnancies, human peripheral blood Tregs and sera from normal pregnancy, preeclampsia and gestational diabetes. In Chapter 2, we show that uterine regulatory T cells amplify and acquire an inflammatory phenotype in response to the TLR-3 agonist and cause pregnancy demise in IL-10-/- and wild-type (WT) mice. In Chapter 3, we present for the first time that peripheral blood Tregs from GDM patients present an “exhausted” phenotype and express the programmed death receptor (PD-1). Tregs from GDM lose CD25 and Foxp3 expression upon overnight culturing which can be partially rescued by TGF-β, IL-2, or PD-1 blockade. This phenotype was not observed in Tregs from normal pregnancy. In Chapter 4, we describe that hCG produced in preeclampsia is inactive and does not support angiogenesis and recruitment of Tregs to the uterus in the “humanized” mouse model of preeclampsia. Collectively, the results presented in this thesis provide novel pathways by which regulatory T cells can present themselves as foes of normal pregnancy. Advisors/Committee Members: Sharma, Surendra (Director), Ayala, alfred (Reader), Fast, Loren (Reader), Reichner, Jonathan (Reader), Golos, Thaddeus (Reader).

Subjects/Keywords: Regulatory T cells

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APA (6^th Edition):

Nevers, T. A. (2012). Inflammatory and dysfunctional regulatory T cells in adverse pregnancy outcomes. (Doctoral Dissertation). Brown University. Retrieved from https://repository.library.brown.edu/studio/item/bdr:297562/

Chicago Manual of Style (16^th Edition):

Nevers, Tania A. “Inflammatory and dysfunctional regulatory T cells in adverse pregnancy outcomes.” 2012. Doctoral Dissertation, Brown University. Accessed February 17, 2020. https://repository.library.brown.edu/studio/item/bdr:297562/.

MLA Handbook (7^th Edition):

Nevers, Tania A. “Inflammatory and dysfunctional regulatory T cells in adverse pregnancy outcomes.” 2012. Web. 17 Feb 2020.

Vancouver:

Nevers TA. Inflammatory and dysfunctional regulatory T cells in adverse pregnancy outcomes. [Internet] [Doctoral dissertation]. Brown University; 2012. [cited 2020 Feb 17]. Available from: https://repository.library.brown.edu/studio/item/bdr:297562/.

Council of Science Editors:

Nevers TA. Inflammatory and dysfunctional regulatory T cells in adverse pregnancy outcomes. [Doctoral Dissertation]. Brown University; 2012. Available from: https://repository.library.brown.edu/studio/item/bdr:297562/

7. Ruiz, Victoria E. Immune response to Helicobacter pylori infection in the gastric cancer prone p27-deficient mouse model.

Degree: PhD, Pathobiology, 2012, Brown University

URL: https://repository.library.brown.edu/studio/item/bdr:297572/

► Helicobacter pylori infection is associated with severe chronic inflammation, however the host immune response is unable to clear the bacterium. Thymus derived lymphocyte populations such… (more)

▼ Helicobacter pylori infection is associated with severe chronic inflammation, however the host immune response is unable to clear the bacterium. Thymus derived lymphocyte populations such as T-helper 1, T-helper 17, and T-regulatory lymphocytes are known to promote chronicity of infection as well as increased gastric pathology. It is yet to be established how these immune cells interact in the gastric environment during H. pylori infection and how changes in the gastric T- lymphocyte cell repertoire may lead gastric cancer associated pathology. To first characterize gastric T-lymphocyte populations, a gastric lymphocyte isolation technique was developed. H. pylori infected murine gastric tissue was digested with EDTA/DTT and collagenase IV. To enrich for gastric lymphocyte populations, a lympholyte M gradient was used. This protocol successfully isolated 1x 106 viable lymphocytes from the gastric compartment to be used for ex vivo experiments and subsequent immunophenotyping using flow cytometric analysis. Using this procedure a 2-fold increase of CD8+ IFNg-expressing lymphocytes was observed in the gastric compartment during H. pylori infection. Implementing the established gastric lymphocyte isolation technique, gastric T-helper and T-regulatory lymphocyte populations were evaluated in p27-deficient mice. These mice develop gastric cancer a year after H. pylori infection, mimicking the human clinical course of disease. Thus providing a suitable model to study H. pylori induced immunopathogenesis. This work demonstrated that H. pylori infected p27-deficient mice displayed an increased frequency of CD4+ IFNγ+ T helper populations in the stomach, spleen and mesenteric lymph nodes. Additionally, infected p27-deficient mice exhibited elevated protein and transcript levels of pro-inflammatory cytokines IFNγ, TNFα, ΙL-12p40 and chemokine, RANTES. Along with a significant Th-1 skewed response, p27-deficient mice exhibited decreased H. pylori colonization and increased gastric pathology compared to its wild-type counterparts. This data demonstrates that in p27-deficient mice, H. pylori induces a pro-inflammatory environment by recruiting Th1 cells to the gastric mucosa and other lymphoid compartments. Data suggest that this recruitment, likely mediated by RANTES, may contribute to subsequent gastric pathogenesis and eventual bacterial clearance. Advisors/Committee Members: Moss, Steven (Director), Ayala, Alfred (Reader), Fast, Loren (Reader), Salazar-Mather, Thais (Reader), Perez-Perez, Guillermo (Reader).

Subjects/Keywords: T-helper cells

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APA (6^th Edition):

Ruiz, V. E. (2012). Immune response to Helicobacter pylori infection in the gastric cancer prone p27-deficient mouse model. (Doctoral Dissertation). Brown University. Retrieved from https://repository.library.brown.edu/studio/item/bdr:297572/

Chicago Manual of Style (16^th Edition):

Ruiz, Victoria E. “Immune response to Helicobacter pylori infection in the gastric cancer prone p27-deficient mouse model.” 2012. Doctoral Dissertation, Brown University. Accessed February 17, 2020. https://repository.library.brown.edu/studio/item/bdr:297572/.

MLA Handbook (7^th Edition):

Ruiz, Victoria E. “Immune response to Helicobacter pylori infection in the gastric cancer prone p27-deficient mouse model.” 2012. Web. 17 Feb 2020.

Vancouver:

Ruiz VE. Immune response to Helicobacter pylori infection in the gastric cancer prone p27-deficient mouse model. [Internet] [Doctoral dissertation]. Brown University; 2012. [cited 2020 Feb 17]. Available from: https://repository.library.brown.edu/studio/item/bdr:297572/.

Council of Science Editors:

Ruiz VE. Immune response to Helicobacter pylori infection in the gastric cancer prone p27-deficient mouse model. [Doctoral Dissertation]. Brown University; 2012. Available from: https://repository.library.brown.edu/studio/item/bdr:297572/

University of Gothenburg / Göteborgs Universitet

8. Alsén, Samuel. Dendritic cells and B cells in effector T cells decisions - promotion of antibody induction in lymphoid tissues or gut homing.

Degree: 2018, University of Gothenburg / Göteborgs Universitet

URL: http://hdl.handle.net/2077/55393

► Abstract CD4+ T cells are principal cells of the adaptive immune system, equipped with the ability to boost innate immune cells and aid B cells… (more)

Subjects/Keywords: Immunology; T cells; T follicular helper cells; dendritic cells

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APA (6^th Edition):

Alsén, S. (2018). Dendritic cells and B cells in effector T cells decisions - promotion of antibody induction in lymphoid tissues or gut homing. (Thesis). University of Gothenburg / Göteborgs Universitet. Retrieved from http://hdl.handle.net/2077/55393

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):

Alsén, Samuel. “Dendritic cells and B cells in effector T cells decisions - promotion of antibody induction in lymphoid tissues or gut homing.” 2018. Thesis, University of Gothenburg / Göteborgs Universitet. Accessed February 17, 2020. http://hdl.handle.net/2077/55393.

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

MLA Handbook (7^th Edition):

Alsén, Samuel. “Dendritic cells and B cells in effector T cells decisions - promotion of antibody induction in lymphoid tissues or gut homing.” 2018. Web. 17 Feb 2020.

Vancouver:

Alsén S. Dendritic cells and B cells in effector T cells decisions - promotion of antibody induction in lymphoid tissues or gut homing. [Internet] [Thesis]. University of Gothenburg / Göteborgs Universitet; 2018. [cited 2020 Feb 17]. Available from: http://hdl.handle.net/2077/55393.

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

Council of Science Editors:

Alsén S. Dendritic cells and B cells in effector T cells decisions - promotion of antibody induction in lymphoid tissues or gut homing. [Thesis]. University of Gothenburg / Göteborgs Universitet; 2018. Available from: http://hdl.handle.net/2077/55393

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

Queen Mary, University of London

9. Kishore, Madhav. The role of co-stimulatory receptors in the regulation of regulatory T cell migration.

Degree: PhD, 2016, Queen Mary, University of London

URL: http://qmro.qmul.ac.uk/xmlui/handle/123456789/12869 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.775244

► Once an immune response is initiated, a combination of several mechanisms coordinates and directs the homing of T cells to their target tissue. Co-stimulatory receptors… (more)

▼ Once an immune response is initiated, a combination of several mechanisms coordinates and directs the homing of T cells to their target tissue. Co-stimulatory receptors expressed on the surface of T lymphocytes are known to actively regulate T cell motility and thus are crucial for regulating T cell migration. The B7 co-stimulatory receptor family members CD28 and CTLA-4 are well known to positively and negatively regulate effector T cell motility respectively. However, their effect on motility and subsequently migration has not been specifically studied in regulatory T cells (Tregs). Tregs are a CD4+ T cell subset fundamental for maintaining immune homeostasis and their role in controlling autoimmunity has been well established through a variety of experimental animal models. Tregs differ from conventional T cells in their expression of CTLA-4. While conventional T cells express CTLA-4 only after activation, Tregs are known to express this negative co-stimulatory receptor constitutively. Additionally, Tregs display a distinct metabolic phenotype to that of conventional T cells. This thesis examines the impact of both co-stimulatory receptors on Treg migration while taking in account the consequences of the concomitant delivery of signals from both. The data in this study suggests that glycolysis, rather than lipid oxidation induced by CD28 promotes Treg migration through glycolytic enzymes including glucokinase, whose expression in T cells was previously unknown. In contrast, CTLA-4 inhibits CD28 induced Treg migration via inhibition of these glycolytic enzymes. The therapeutic implications of these results in the context of disease and transplantation are discussed. CD31, an IgG like molecule, is expressed on a number of leukocytes including lymphocytes. In T cells, CD31 inhibits activation by recruiting phosphatases through its cytoplasmic ITIM domains and has thus been described as a co-inhibitory receptor. The role of this co-receptor in the regulation of T cell migration is investigated in the last part of this thesis. Our observations suggest that CD31 selectively signals in activated T cells to regulate their migration in response to inflammatory chemokines, revealing an additional role of this receptor in regulating T cell-mediated inflammation.

Subjects/Keywords: Medicine; regulatory T cells; T cell migration

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APA (6^th Edition):

Kishore, M. (2016). The role of co-stimulatory receptors in the regulation of regulatory T cell migration. (Doctoral Dissertation). Queen Mary, University of London. Retrieved from http://qmro.qmul.ac.uk/xmlui/handle/123456789/12869 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.775244

Chicago Manual of Style (16^th Edition):

Kishore, Madhav. “The role of co-stimulatory receptors in the regulation of regulatory T cell migration.” 2016. Doctoral Dissertation, Queen Mary, University of London. Accessed February 17, 2020. http://qmro.qmul.ac.uk/xmlui/handle/123456789/12869 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.775244.

MLA Handbook (7^th Edition):

Kishore, Madhav. “The role of co-stimulatory receptors in the regulation of regulatory T cell migration.” 2016. Web. 17 Feb 2020.

Vancouver:

Kishore M. The role of co-stimulatory receptors in the regulation of regulatory T cell migration. [Internet] [Doctoral dissertation]. Queen Mary, University of London; 2016. [cited 2020 Feb 17]. Available from: http://qmro.qmul.ac.uk/xmlui/handle/123456789/12869 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.775244.

Council of Science Editors:

Kishore M. The role of co-stimulatory receptors in the regulation of regulatory T cell migration. [Doctoral Dissertation]. Queen Mary, University of London; 2016. Available from: http://qmro.qmul.ac.uk/xmlui/handle/123456789/12869 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.775244

Loyola University Chicago

10. Chandrasekaran, Uma. Phospholipase D Signaling in T Cells.

Degree: PhD, Microbiology and Immunology, 2010, Loyola University Chicago

URL: https://ecommons.luc.edu/luc_diss/162

► Antigen stimulation of T lymphocytes induces the activation of phospholipase D (PLD) signaling. Phospholipase D (PLD) is a phosphodiesterase that catalyzes the conversion of… (more)

▼ Antigen stimulation of T lymphocytes induces the activation of phospholipase D (PLD) signaling. Phospholipase D (PLD) is a phosphodiesterase that catalyzes the conversion of phosphatidyl choline (PC) to phosphatidic acid (PA). PA is an important lipid second messenger and is known to mediate a variety of cellular functions. However, the specific role of PA in T lymphocytes has not been established. Previous studies indicated differential requirement for TCR induced PLD signaling in regulatory and non-regulatory T cells. Inhibition of TCR induced PLD signal preferentially suppressed the growth of non-regulatory T cells while allowing the proliferation of regulatory T cells in the presence of exogenous IL-2. Based on this observation, we hypothesized that PLD signaling is a critical factor that balances the population dynamics between regulatory and non-regulatory T cells. For my dissertation work, I focused on elucidating the functional and molecular regulation of PLD signaling in T cells. In this study, we identified that various exogenous (alcohol and Clostridium difficile toxin) and endogenous factors (adenosine) modulate PLD signaling altering the population dynamics of regulatory and non-regulatory T cells. PLD has two isoforms namely PLD1 and PLD2 expressed in mammalian cells. These isoforms are 50% identical and have distinct localization in the cell. PLD1 has peri-nuclear localization while PLD2 localizes to the plasma membrane. Molecular analysis of PLD1 and PLD2 using domain deletion suggested that a region unique to PLD1 known as the `loop' confers the distinct peri-nuclear localization of PLD1. Further, we addressed the specific function of PLD2 in CD4 T cells using PLD2 knock out mice. We found that PLD2 is dispensable for T cell activation and proliferation but might play an important role in effector T cell differentiation. The results from this study delineate some of the functions of PLD signaling in T cells and provide insight into immunological regulation during T cell activation.

Subjects/Keywords: CD4 T CELLS; EFFECTOR T CELLS; PLD SIGNALING; REGULATORY T CELLS; Immunology and Infectious Disease

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APA (6^th Edition):

Chandrasekaran, U. (2010). Phospholipase D Signaling in T Cells. (Doctoral Dissertation). Loyola University Chicago. Retrieved from https://ecommons.luc.edu/luc_diss/162

Chicago Manual of Style (16^th Edition):

Chandrasekaran, Uma. “Phospholipase D Signaling in T Cells.” 2010. Doctoral Dissertation, Loyola University Chicago. Accessed February 17, 2020. https://ecommons.luc.edu/luc_diss/162.

MLA Handbook (7^th Edition):

Chandrasekaran, Uma. “Phospholipase D Signaling in T Cells.” 2010. Web. 17 Feb 2020.

Vancouver:

Chandrasekaran U. Phospholipase D Signaling in T Cells. [Internet] [Doctoral dissertation]. Loyola University Chicago; 2010. [cited 2020 Feb 17]. Available from: https://ecommons.luc.edu/luc_diss/162.

Council of Science Editors:

Chandrasekaran U. Phospholipase D Signaling in T Cells. [Doctoral Dissertation]. Loyola University Chicago; 2010. Available from: https://ecommons.luc.edu/luc_diss/162

University of Oxford

11. Huo, Jiandong. System-level analysis of early signalling in T cells.

Degree: PhD, 2012, University of Oxford

URL: http://ora.ox.ac.uk/objects/uuid:dcff1741-bd39-4b5b-a11b-99277d55890d ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.588401

► The prevailing view of signal transduction is that it proceeds through the linear relay of information via sequential bimolecular interactions, involving, for example, Src homology… (more)

▼ The prevailing view of signal transduction is that it proceeds through the linear relay of information via sequential bimolecular interactions, involving, for example, Src homology (SH) 2 domains. It has been assumed that such interactions are highly selective, i.e. that the affinities of these interactions are several orders of magnitude higher than that for non-specific interactions. However, recent studies have suggested that the difference in affinities between so-called specific and non-specific interactions is not sufficient to support such a proposal. This therefore raises the question of how signalling pathway specificity is generated at all. To address this, we have taken a systems approach by expressing and purifying >90% of the SH2 domains identified in a T cell line using a next-generation sequencing-based transcriptomic analysis, and performed a systematic survey of the interaction of these SH2 domains with a set of potential phosphorylated peptides derived from the key signalling receptors of the T cell (including CD28, CTLA-4, PD-1, ICOS, BTLA, LAT and the CD3 subunits of the TCR complex), using surface plasmon resonance-based binding assays. Our results show that, instead of being highly selective for certain SH2 domains, the T cell-expressed receptors are very cross-reactive, such that each receptor is found to interact with ~50 different SH2 domains on average. In silico analysis based on these results confirms the expectation that affinity itself is not the sole determining factor for receptor specificity. Further exploration of the system using in silico simulations incorporating the absolute concentrations of SH2 domain-containing proteins measured in T cells using a proteomics-based approach, suggests instead that the specificity of SH2 domain recruitment by T-cell receptors is the result of systems effects, with expression levels of the signalling proteins being a major factor. Surprisingly, LCK, the most highly expressed SH2 domain in resting Jurkat, is predicted to dominate the binding of most receptors, suggesting a novel mechanism of Src kinase activation and function.

Subjects/Keywords: 571.966; Immunology; signalling; T cells

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APA (6^th Edition):

Huo, J. (2012). System-level analysis of early signalling in T cells. (Doctoral Dissertation). University of Oxford. Retrieved from http://ora.ox.ac.uk/objects/uuid:dcff1741-bd39-4b5b-a11b-99277d55890d ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.588401

Chicago Manual of Style (16^th Edition):

Huo, Jiandong. “System-level analysis of early signalling in T cells.” 2012. Doctoral Dissertation, University of Oxford. Accessed February 17, 2020. http://ora.ox.ac.uk/objects/uuid:dcff1741-bd39-4b5b-a11b-99277d55890d ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.588401.

MLA Handbook (7^th Edition):

Huo, Jiandong. “System-level analysis of early signalling in T cells.” 2012. Web. 17 Feb 2020.

Vancouver:

Huo J. System-level analysis of early signalling in T cells. [Internet] [Doctoral dissertation]. University of Oxford; 2012. [cited 2020 Feb 17]. Available from: http://ora.ox.ac.uk/objects/uuid:dcff1741-bd39-4b5b-a11b-99277d55890d ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.588401.

Council of Science Editors:

Huo J. System-level analysis of early signalling in T cells. [Doctoral Dissertation]. University of Oxford; 2012. Available from: http://ora.ox.ac.uk/objects/uuid:dcff1741-bd39-4b5b-a11b-99277d55890d ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.588401

University of Alberta

12. Hockley, Deanna L. Co-stimulator contributions in CD8+ T cell differentiation.

Degree: PhD, Department of Medical Microbiology and Immunology, 2012, University of Alberta

URL: https://era.library.ualberta.ca/files/f4752h04p

► The adaptive immune response against intracellular pathogens is largely mediated by CD8+ T lymphocytes. The clonal expansion and expression of cytolytic and immune stimulatory proteins… (more)

▼ The adaptive immune response against intracellular pathogens is largely mediated by CD8+ T lymphocytes. The clonal expansion and expression of cytolytic and immune stimulatory proteins by CD8+ T cells is responsible for their protective immune function. Prior to exhibiting effector activity, CD8+ T cells exist in a naïve state and require three stimulatory signals for their optimal activation including the recognition of antigen, co-stimulator ligand engagement, and the presence of pro-inflammatory cytokines. When these activation requirements are met, CD8+ T cells undergo a well described series of events including clonal expansion, cellular contraction, memory generation, and memory maintenance. The memory CD8+ T cell population generated can survive for the life-time of the host, and provides more rapid and robust protection upon re-infection then their naïve precursors. While some factors that induce this sequence of events have been identified, the role of co-stimulation remains relatively undefined. This is due to the large number of co-stimulator receptors expressed by CD8+ T cells that may be ligated individually and/or in combination, to instruct the development of specific effector and memory CD8+ T cell phenotypes. Using a bead-based ligand presentation system, I investigated the role of co-stimulation in directing naïve CD8+ T cell activation, and the generation of T cell populations with distinct effector and memory fates. I identified ICAM-1 as the stimulatory molecule best able to induce naïve CD8+ T cell proliferation and expression of the effector molecule granzyme B, while co-stimulation through CD28 was required to induce IFN-γ. When provided in combination however, B7.1 and ICAM-1 co-stimulation generated CD8+ T cells which were highly cytolytic and expressed high amounts of IFN-γ. These cells also exhibited enhanced survival once activated, with sustained expression of anti-apoptotic proteins and secretion of high amounts of IL-2, resulting in these cells exhibiting a terminal effector phenotype. While other co-stimulator combinations also enhanced CD8+ T cell survival to some degree, their ability to sustain high expression of IL-2 was limited. This translated into less potent effector responses and preferential memory precursor development based on transcription factor expression.

Subjects/Keywords: Immunology; T cells; Co-stimulation

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APA (6^th Edition):

Hockley, D. L. (2012). Co-stimulator contributions in CD8+ T cell differentiation. (Doctoral Dissertation). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/f4752h04p

Chicago Manual of Style (16^th Edition):

Hockley, Deanna L. “Co-stimulator contributions in CD8+ T cell differentiation.” 2012. Doctoral Dissertation, University of Alberta. Accessed February 17, 2020. https://era.library.ualberta.ca/files/f4752h04p.

MLA Handbook (7^th Edition):

Hockley, Deanna L. “Co-stimulator contributions in CD8+ T cell differentiation.” 2012. Web. 17 Feb 2020.

Vancouver:

Hockley DL. Co-stimulator contributions in CD8+ T cell differentiation. [Internet] [Doctoral dissertation]. University of Alberta; 2012. [cited 2020 Feb 17]. Available from: https://era.library.ualberta.ca/files/f4752h04p.

Council of Science Editors:

Hockley DL. Co-stimulator contributions in CD8+ T cell differentiation. [Doctoral Dissertation]. University of Alberta; 2012. Available from: https://era.library.ualberta.ca/files/f4752h04p

University of Alberta

13. He, Jinshu. Regulation of FasL expression and trafficking in cytotoxic T lymphocytes.

Degree: PhD, Department of Medical Microbiology and Immunology, 2009, University of Alberta

URL: https://era.library.ualberta.ca/files/4x51hj17q

► Cytotoxic T lymphocytes (CTL) are differentiated CD8+ T cells that eliminate virally infected cells and tumor cells. CTL lyse target cells by at least two… (more)

Subjects/Keywords: cytotoxicity; T cells; Fas ligand

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APA (6^th Edition):

He, J. (2009). Regulation of FasL expression and trafficking in cytotoxic T lymphocytes. (Doctoral Dissertation). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/4x51hj17q

Chicago Manual of Style (16^th Edition):

He, Jinshu. “Regulation of FasL expression and trafficking in cytotoxic T lymphocytes.” 2009. Doctoral Dissertation, University of Alberta. Accessed February 17, 2020. https://era.library.ualberta.ca/files/4x51hj17q.

MLA Handbook (7^th Edition):

He, Jinshu. “Regulation of FasL expression and trafficking in cytotoxic T lymphocytes.” 2009. Web. 17 Feb 2020.

Vancouver:

He J. Regulation of FasL expression and trafficking in cytotoxic T lymphocytes. [Internet] [Doctoral dissertation]. University of Alberta; 2009. [cited 2020 Feb 17]. Available from: https://era.library.ualberta.ca/files/4x51hj17q.

Council of Science Editors:

He J. Regulation of FasL expression and trafficking in cytotoxic T lymphocytes. [Doctoral Dissertation]. University of Alberta; 2009. Available from: https://era.library.ualberta.ca/files/4x51hj17q

14. 佐伯, 晃一. THEORETICAL STUDIES OF SELF-TOLERANCE : REGULATORY T CELLS AND ANERGY : 自己寛容に関する理論的研究 : 制御性Ｔ細胞とアナジーについて.

Degree: 博士（理学）, 2013, Kyushu University / 九州大学

URL: http://hdl.handle.net/2324/21712 ; http://dx.doi.org/10.15017/21712

自己寛容とは免疫システムが自分の体に対して反応を示さない状態のことである。これは生物が生まれながらに持っている性質ではなく、成立にはその為のメカニズムが必要である。例えば、獲得免疫系を担うリンパ球はランダムに生成された受容体を用いて抗原の認識を行うため、自分の体由来の抗原を認識するリンパ球も作られる。そのため成熟前に受容体をチェックし、自己抗原を認識するものは排除する(負の選択)機構が存在する。しかしながら、このチェック機構だけでは不十分であり、リンパ球の成熟後に末梢において自己寛容を保証するメカニズムがあることが知られている。自己寛容の破綻は自己免疫疾患につながるため、メカニズムの理解は医学的な観点からも注目を集めている。本論文では、自己寛容の成立に関わっている二つの機構、制御性T細胞とアナジーに着目しそれらの意義ついて数理モデルを用いて議論した。二つの機構は常に有益となるわけではなく、幾つかの条件下で有利に働くことが分かった。 Advisors/Committee Members: 巌佐, 庸.

Subjects/Keywords: self-tolerance; regulatory T cells

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APA (6^th Edition):

佐伯, �. (2013). THEORETICAL STUDIES OF SELF-TOLERANCE : REGULATORY T CELLS AND ANERGY : 自己寛容に関する理論的研究 : 制御性Ｔ細胞とアナジーについて. (Thesis). Kyushu University / 九州大学. Retrieved from http://hdl.handle.net/2324/21712 ; http://dx.doi.org/10.15017/21712

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):

佐伯, 晃一. “THEORETICAL STUDIES OF SELF-TOLERANCE : REGULATORY T CELLS AND ANERGY : 自己寛容に関する理論的研究 : 制御性Ｔ細胞とアナジーについて.” 2013. Thesis, Kyushu University / 九州大学. Accessed February 17, 2020. http://hdl.handle.net/2324/21712 ; http://dx.doi.org/10.15017/21712.

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

MLA Handbook (7^th Edition):

佐伯, 晃一. “THEORETICAL STUDIES OF SELF-TOLERANCE : REGULATORY T CELLS AND ANERGY : 自己寛容に関する理論的研究 : 制御性Ｔ細胞とアナジーについて.” 2013. Web. 17 Feb 2020.

Vancouver:

佐伯 �. THEORETICAL STUDIES OF SELF-TOLERANCE : REGULATORY T CELLS AND ANERGY : 自己寛容に関する理論的研究 : 制御性Ｔ細胞とアナジーについて. [Internet] [Thesis]. Kyushu University / 九州大学; 2013. [cited 2020 Feb 17]. Available from: http://hdl.handle.net/2324/21712 ; http://dx.doi.org/10.15017/21712.

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

Council of Science Editors:

佐伯 �. THEORETICAL STUDIES OF SELF-TOLERANCE : REGULATORY T CELLS AND ANERGY : 自己寛容に関する理論的研究 : 制御性Ｔ細胞とアナジーについて. [Thesis]. Kyushu University / 九州大学; 2013. Available from: http://hdl.handle.net/2324/21712 ; http://dx.doi.org/10.15017/21712

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

University of Aberdeen

15. Whibley, Natasha. The role of effector and regulatory helper T cells in a murine model of systemic Candida albicans infection.

Degree: PhD, 2013, University of Aberdeen

URL: http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=192231 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.569637

► Diseases caused by fungi are increasing worldwide and are often associated with high mortality rates. In particular, the normally harmless commensal Candida albicans can cause… (more)

Subjects/Keywords: 610; Candida albicans; T-cells

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APA (6^th Edition):

Whibley, N. (2013). The role of effector and regulatory helper T cells in a murine model of systemic Candida albicans infection. (Doctoral Dissertation). University of Aberdeen. Retrieved from http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=192231 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.569637

Chicago Manual of Style (16^th Edition):

Whibley, Natasha. “The role of effector and regulatory helper T cells in a murine model of systemic Candida albicans infection.” 2013. Doctoral Dissertation, University of Aberdeen. Accessed February 17, 2020. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=192231 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.569637.

MLA Handbook (7^th Edition):

Whibley, Natasha. “The role of effector and regulatory helper T cells in a murine model of systemic Candida albicans infection.” 2013. Web. 17 Feb 2020.

Vancouver:

Whibley N. The role of effector and regulatory helper T cells in a murine model of systemic Candida albicans infection. [Internet] [Doctoral dissertation]. University of Aberdeen; 2013. [cited 2020 Feb 17]. Available from: http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=192231 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.569637.

Council of Science Editors:

Whibley N. The role of effector and regulatory helper T cells in a murine model of systemic Candida albicans infection. [Doctoral Dissertation]. University of Aberdeen; 2013. Available from: http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=192231 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.569637

University of Aberdeen

16. Pappalardo, Angela. Defining the role of γδ cells in bone loss associated with chronic inflammation.

Degree: PhD, 2013, University of Aberdeen

URL: http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=203414 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.589513

► The extensive infiltration of immune cells in the joints of patients affected by rheumatoid arthritis (RA), and the subsequent production of pro-inflammatory cytokines triggers bone… (more)

Subjects/Keywords: 616.7; Osteoclast inhibition; T cells

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APA (6^th Edition):

Pappalardo, A. (2013). Defining the role of γδ cells in bone loss associated with chronic inflammation. (Doctoral Dissertation). University of Aberdeen. Retrieved from http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=203414 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.589513

Chicago Manual of Style (16^th Edition):

Pappalardo, Angela. “Defining the role of γδ cells in bone loss associated with chronic inflammation.” 2013. Doctoral Dissertation, University of Aberdeen. Accessed February 17, 2020. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=203414 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.589513.

MLA Handbook (7^th Edition):

Pappalardo, Angela. “Defining the role of γδ cells in bone loss associated with chronic inflammation.” 2013. Web. 17 Feb 2020.

Vancouver:

Pappalardo A. Defining the role of γδ cells in bone loss associated with chronic inflammation. [Internet] [Doctoral dissertation]. University of Aberdeen; 2013. [cited 2020 Feb 17]. Available from: http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=203414 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.589513.

Council of Science Editors:

Pappalardo A. Defining the role of γδ cells in bone loss associated with chronic inflammation. [Doctoral Dissertation]. University of Aberdeen; 2013. Available from: http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=203414 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.589513

Oregon State University

17. Maxwell, Joseph R. The role of costimulation and adjuvants in the development of T cell effector and memory responses.

Degree: PhD, Microbiology, 2001, Oregon State University

URL: http://hdl.handle.net/1957/32495

► T cells are one of the key cells in the immune system. Although they are not the first line of defense against a pathogen, their… (more)

▼ T cells are one of the key cells in the immune system. Although they are not the first line of defense against a pathogen, their functions can greatly enhance the phagocytosis and destruction of pathogens as well as the development of antibody responses. Furthermore, even when responding T cells have facilitated the clearance of the pathogen, they can avoid death to become long-lived cells that "remember" encountering the pathogen for years afterward. This long-term memory allows subsequent immune responses to improve with each exposure, ultimately preventing disease upon reinfection. The activation of these T cells depends on specific recognition of antigen along with a costimulatory signal. This activation process is well studied, but not completely understood. Additionally, the mechanism behind memory T cell development is still very much unknown. In the work presented in this thesis, delivery of costimulatory signals via CD4O and 0X40 were studied using an in vivo superantigen (SAg) model of T cell stimulation. In the context of this two-signal (SAg + costimulation) model, both CD4O and OX40 could deliver signals that enhanced SAg-reactive T cell clonal expansion, but they could only partially prevent T cell death. Coadministration of the inflammatory agent lipopolysaccharide (LPS), however, could keep increased responder T cell populations alive for at least two months. Interestingly, this three-signal (SAg + costimulation + LPS) induced survival was not dependent on proinflammatory cytokines or activation of the transcription factor NF-KB, but was sensitive to the immunosuppressant cyclosporin A (CsA). The mode of action of CsA may point to the mechanism driving long-term T cell survival. Additionally, examination of early time points after three-signal stimulation suggested more clues to the mechanism of survival induction. The cytokines IL-2 and TNF-α seem to be involved early on, but for now, little is known about their complete role. Thus, the goal of this work was to investigate the costimulatory and adjuvant-mediated signals required for memory T cell development. Ultimately, an understanding of how memory T cells can be generated could be used to enhance vaccine efficacy or shut off autoimmune conditions. Advisors/Committee Members: Vella, Anthony T. (advisor).

Subjects/Keywords: T cells

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APA (6^th Edition):

Maxwell, J. R. (2001). The role of costimulation and adjuvants in the development of T cell effector and memory responses. (Doctoral Dissertation). Oregon State University. Retrieved from http://hdl.handle.net/1957/32495

Chicago Manual of Style (16^th Edition):

Maxwell, Joseph R. “The role of costimulation and adjuvants in the development of T cell effector and memory responses.” 2001. Doctoral Dissertation, Oregon State University. Accessed February 17, 2020. http://hdl.handle.net/1957/32495.

MLA Handbook (7^th Edition):

Maxwell, Joseph R. “The role of costimulation and adjuvants in the development of T cell effector and memory responses.” 2001. Web. 17 Feb 2020.

Vancouver:

Maxwell JR. The role of costimulation and adjuvants in the development of T cell effector and memory responses. [Internet] [Doctoral dissertation]. Oregon State University; 2001. [cited 2020 Feb 17]. Available from: http://hdl.handle.net/1957/32495.

Council of Science Editors:

Maxwell JR. The role of costimulation and adjuvants in the development of T cell effector and memory responses. [Doctoral Dissertation]. Oregon State University; 2001. Available from: http://hdl.handle.net/1957/32495

University of Hong Kong

18. Guan, Jing. The role of virus-specific human T cells in influenza A virus infection.

Degree: M. Phil., 2011, University of Hong Kong

URL: Guan, J. [管静]. (2011). The role of virus-specific human T cells in influenza A virus infection. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4729546 ; http://dx.doi.org/10.5353/th_b4729546 ; http://hdl.handle.net/10722/208423

► Influenza A virus infection is a major cause of human morbidity and mortality. T cell immunity is believed to play critical roles for host defenses… (more)

Subjects/Keywords: Influenza A virus; T-cells

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APA (6^th Edition):

Guan, J. (2011). The role of virus-specific human T cells in influenza A virus infection. (Masters Thesis). University of Hong Kong. Retrieved from Guan, J. [管静]. (2011). The role of virus-specific human T cells in influenza A virus infection. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4729546 ; http://dx.doi.org/10.5353/th_b4729546 ; http://hdl.handle.net/10722/208423

Chicago Manual of Style (16^th Edition):

Guan, Jing. “The role of virus-specific human T cells in influenza A virus infection.” 2011. Masters Thesis, University of Hong Kong. Accessed February 17, 2020. Guan, J. [管静]. (2011). The role of virus-specific human T cells in influenza A virus infection. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4729546 ; http://dx.doi.org/10.5353/th_b4729546 ; http://hdl.handle.net/10722/208423.

MLA Handbook (7^th Edition):

Guan, Jing. “The role of virus-specific human T cells in influenza A virus infection.” 2011. Web. 17 Feb 2020.

Vancouver:

Guan J. The role of virus-specific human T cells in influenza A virus infection. [Internet] [Masters thesis]. University of Hong Kong; 2011. [cited 2020 Feb 17]. Available from: Guan, J. [管静]. (2011). The role of virus-specific human T cells in influenza A virus infection. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4729546 ; http://dx.doi.org/10.5353/th_b4729546 ; http://hdl.handle.net/10722/208423.

Council of Science Editors:

Guan J. The role of virus-specific human T cells in influenza A virus infection. [Masters Thesis]. University of Hong Kong; 2011. Available from: Guan, J. [管静]. (2011). The role of virus-specific human T cells in influenza A virus infection. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4729546 ; http://dx.doi.org/10.5353/th_b4729546 ; http://hdl.handle.net/10722/208423

University of Hong Kong

19. Sung, Ying-ju, Cecilia. Reuglation of T helper 17 by bacteria : an approach for the treatment of hepatocellular carcinoma.

Degree: PhD, 2014, University of Hong Kong

URL: Sung, Y. C. [宋穎如]. (2014). Reuglation of T helper 17 by bacteria : an approach for the treatment of hepatocellular carcinoma. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5387993 ; http://dx.doi.org/10.5353/th_b5387993 ; http://hdl.handle.net/10722/208577

► Hepatocellular carcinoma (HCC) is the sixth most common cancer and the second leading cause of cancer-related deaths in the world. It is a disease with… (more)

▼ Hepatocellular carcinoma (HCC) is the sixth most common cancer and the second leading cause of cancer-related deaths in the world. It is a disease with poor prognosis with unsatisfactory long-term survival of patients, and thus new strategies to control this disease are warranted. T helper (Th) 17 cells and IL-17 have recently been detected with increased frequency in a number of tumors including HCC. Its role in tumor remains controversial but its presence in HCC has been linked to disease progression, possibly involving angiogenesis. Th17 cells could be homed to inflammatory sites such as tumor microenvironment via CCR6/CCL20 axis and expand locally, and studies from other inflammatory diseases such as autoimmune disease has shown that the gut is the potential source of Th17, where its induction is affected by signals from gut microbiota. Yet this link is not yet shown in extra-intestinal tumors. Probiotics are living microorganisms, which when administered in adequate amounts confer a health benefit on the host. They have been reported to relieve chronic inflammatory diseases in animal and in human intervention studies. It is believed that probiotics regulate signals to gut antigen-presenting cells, which act as the pivot in modulating the systemic immune responses and inactivated bacteria also exhibited immunomodulatory effects in this regard. Accordingly, it was hypothesized that oral feeding of probiotics to HCCbearing animals may affect Th17 polarization and distribution and thereby modulate tumor microenvironment, which may have beneficial effect in tumor development, possibly via affecting angiogenesis. To address this hypothesis, wild-type C57BL/6 mice were fed with different heat-inactivated or viable probiotics– Lactobacillus rhamnosus GG (LGG), Escherichia coli Nissle 1917 (EcN), VSL#3 or mixture of probiotics − Prohep (heat-inactivated LGG, heatinactivated VSL#3 and viable EcN) either one week in advance or at the time of subcutaneous tumor inoculation. Probiotic feeding had improved survival in tumor-bearing mice, slowed down tumor growth and reduced tumor burden when monitored for 38 days. Probiotics showed better efficacy when feeding was given in advance. The anti-tumor effect was related to reduced angiogenesis and reduced IL-17 serum and gene expression within tumor. The mechanistic link between IL-17 modulation and tumor development was further studied in animals by IL-17 neutralization. The anti-tumor efficacy of probiotics, in relation to tumor growth and angiogenesis, was lost after IL-17 neutralization, which was linked to recruitment of myeloid suppressor cells. Since cells from both adaptive and innate immune systems could secrete IL-17, the source of IL-17 production was then identified, and found that Th17 was the major IL-17 secretor being modulated by probiotic feeding. Reduced homing of Th17 to tumor via circulation, with a tendency being recruited from gut was observed. Probiotics-mediated Th17 cell modulation in the gut by inducing the skewing of IL-10 secreting type1…

Subjects/Keywords: Liver - Cancer - Treatment; T cells

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APA (6^th Edition):

Sung, Ying-ju, C. (2014). Reuglation of T helper 17 by bacteria : an approach for the treatment of hepatocellular carcinoma. (Doctoral Dissertation). University of Hong Kong. Retrieved from Sung, Y. C. [宋穎如]. (2014). Reuglation of T helper 17 by bacteria : an approach for the treatment of hepatocellular carcinoma. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5387993 ; http://dx.doi.org/10.5353/th_b5387993 ; http://hdl.handle.net/10722/208577

Chicago Manual of Style (16^th Edition):

Sung, Ying-ju, Cecilia. “Reuglation of T helper 17 by bacteria : an approach for the treatment of hepatocellular carcinoma.” 2014. Doctoral Dissertation, University of Hong Kong. Accessed February 17, 2020. Sung, Y. C. [宋穎如]. (2014). Reuglation of T helper 17 by bacteria : an approach for the treatment of hepatocellular carcinoma. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5387993 ; http://dx.doi.org/10.5353/th_b5387993 ; http://hdl.handle.net/10722/208577.

MLA Handbook (7^th Edition):

Sung, Ying-ju, Cecilia. “Reuglation of T helper 17 by bacteria : an approach for the treatment of hepatocellular carcinoma.” 2014. Web. 17 Feb 2020.

Vancouver:

Sung, Ying-ju C. Reuglation of T helper 17 by bacteria : an approach for the treatment of hepatocellular carcinoma. [Internet] [Doctoral dissertation]. University of Hong Kong; 2014. [cited 2020 Feb 17]. Available from: Sung, Y. C. [宋穎如]. (2014). Reuglation of T helper 17 by bacteria : an approach for the treatment of hepatocellular carcinoma. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5387993 ; http://dx.doi.org/10.5353/th_b5387993 ; http://hdl.handle.net/10722/208577.

Council of Science Editors:

Sung, Ying-ju C. Reuglation of T helper 17 by bacteria : an approach for the treatment of hepatocellular carcinoma. [Doctoral Dissertation]. University of Hong Kong; 2014. Available from: Sung, Y. C. [宋穎如]. (2014). Reuglation of T helper 17 by bacteria : an approach for the treatment of hepatocellular carcinoma. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5387993 ; http://dx.doi.org/10.5353/th_b5387993 ; http://hdl.handle.net/10722/208577

University of Oxford

20. Subramaniam, Sumithra. The role of CD1a-restricted T cells and phospholipase in allergic disease.

Degree: PhD, 2015, University of Oxford

URL: https://ora.ox.ac.uk/objects/uuid:71354ef8-3048-4869-9fe8-fcfef5b97240 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.730540

► The skin is an important barrier against a range of different environmental challenges. The skin associated immune system is able to detect breaks in the… (more)

Subjects/Keywords: T-cells; Lipids; Immunology; Skin

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APA (6^th Edition):

Subramaniam, S. (2015). The role of CD1a-restricted T cells and phospholipase in allergic disease. (Doctoral Dissertation). University of Oxford. Retrieved from https://ora.ox.ac.uk/objects/uuid:71354ef8-3048-4869-9fe8-fcfef5b97240 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.730540

Chicago Manual of Style (16^th Edition):

Subramaniam, Sumithra. “The role of CD1a-restricted T cells and phospholipase in allergic disease.” 2015. Doctoral Dissertation, University of Oxford. Accessed February 17, 2020. https://ora.ox.ac.uk/objects/uuid:71354ef8-3048-4869-9fe8-fcfef5b97240 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.730540.

MLA Handbook (7^th Edition):

Subramaniam, Sumithra. “The role of CD1a-restricted T cells and phospholipase in allergic disease.” 2015. Web. 17 Feb 2020.

Vancouver:

Subramaniam S. The role of CD1a-restricted T cells and phospholipase in allergic disease. [Internet] [Doctoral dissertation]. University of Oxford; 2015. [cited 2020 Feb 17]. Available from: https://ora.ox.ac.uk/objects/uuid:71354ef8-3048-4869-9fe8-fcfef5b97240 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.730540.

Council of Science Editors:

Subramaniam S. The role of CD1a-restricted T cells and phospholipase in allergic disease. [Doctoral Dissertation]. University of Oxford; 2015. Available from: https://ora.ox.ac.uk/objects/uuid:71354ef8-3048-4869-9fe8-fcfef5b97240 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.730540

University of Hong Kong

21. Zhang, Jing. The immunomodulatory properties of Cordyceps cicadae on resting and proliferating human T-lymphocytes.

Degree: M. Phil., 2012, University of Hong Kong

URL: Zhang, J. [张婧]. (2012). The immunomodulatory properties of Cordyceps cicadae on resting and proliferating human T-lymphocytes. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4961803 ; http://dx.doi.org/10.5353/th_b4961803 ; http://hdl.handle.net/10722/180982

►

Cordyceps cicadae, a parasitic fungus, has been used as a traditional Chinese herb for treatment of illnesses related to immune dysfunction. However, mechanistic actions are… (more)

▼

Cordyceps cicadae, a parasitic fungus, has been used as a traditional Chinese herb for treatment of illnesses related to immune dysfunction. However, mechanistic actions are not entirely clear. The specific aim of the present study is to investigate the immunological mechanisms of C. cicadae on human T lymphocytes in vitro. The two main objectives carried out in the present study in order to achieve the aim are: i. to investigate the immunological effects of the water extract of C.cicadae on human resting and proliferating T lymphocytes; 2. to investigate the adjuvant property of C.cicadae with the immunosuppressant Cyclosporin A (CsA) on the control of human T cells proliferation, cell death and cytokines secretion. C. cicadae has demonstrated a dual effect of enhancing the activity of resting Tlymphocytes and inhibiting that of PHA-stimulated cells. In resting T cells, C. cicadae increased cell activity, cytokines secretion, expression of IL-2α receptor (CD25) and the population of Th17 as well as Treg cells without affecting the cell cycle progression. In the viability and cell death test, C. cicadae has been found not to exert toxicity on T cells. These results reveal the role of C. cicadae as an invigorant to improve the immunity as a whole in healthy individuals. In PHA-stimulated proliferating T-lymphocytes, C. cicadae inhibited the cell proliferation by arresting them at G0/G1 phase and decreasing both S and G2/M phase cell populations. The inhibitory effect was not through the induction of cell death as both PHA- and CsA-induced cell apoptosis and necrosis were reduced by C. cicadae treatment. It was believed that C. cicadae affects the progression of inflammatory responses by selectively suppressing the secretion of Th1 cytokines and enhancing that of Th2 cytokines, but it seemed unable to influence the CD25 expression in PHA- and CsA-treated T cells. An increased population of Treg cells by C. cicadae was also observed in PHA-stimulated T cells. C. cicadae adjuvant to CsA showed greater inhibition of cell proliferation and Th1 cytokines production. However, C. cicadae antagonized the effect of CsA in the secretion of IL-10, a Th2 and Treg cytokine. These results suggest a potential role of C. cicadae as an adjuvantive agent with CsA in the therapy of autoimmune diseases and organ transplantation. Furthermore, C. cicadae demonstrated superior immunomodulatory properties over CsA as it can act selectively between resting and proliferating T cells, and also protect them from apoptosis and necrosis, alleviating the toxic effect caused by CsA. In summary, this study showed the potential of C. cicadae as an immunomodulator from which both healthy individuals and inflammatory disease patients can benefit.

published_or_final_version

Biological Sciences

Master

Master of Philosophy

Subjects/Keywords: Cordyceps - Therapeutic use.; T cells.

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APA (6^th Edition):

Zhang, J. (2012). The immunomodulatory properties of Cordyceps cicadae on resting and proliferating human T-lymphocytes. (Masters Thesis). University of Hong Kong. Retrieved from Zhang, J. [张婧]. (2012). The immunomodulatory properties of Cordyceps cicadae on resting and proliferating human T-lymphocytes. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4961803 ; http://dx.doi.org/10.5353/th_b4961803 ; http://hdl.handle.net/10722/180982

Chicago Manual of Style (16^th Edition):

Zhang, Jing. “The immunomodulatory properties of Cordyceps cicadae on resting and proliferating human T-lymphocytes.” 2012. Masters Thesis, University of Hong Kong. Accessed February 17, 2020. Zhang, J. [张婧]. (2012). The immunomodulatory properties of Cordyceps cicadae on resting and proliferating human T-lymphocytes. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4961803 ; http://dx.doi.org/10.5353/th_b4961803 ; http://hdl.handle.net/10722/180982.

MLA Handbook (7^th Edition):

Zhang, Jing. “The immunomodulatory properties of Cordyceps cicadae on resting and proliferating human T-lymphocytes.” 2012. Web. 17 Feb 2020.

Vancouver:

Zhang J. The immunomodulatory properties of Cordyceps cicadae on resting and proliferating human T-lymphocytes. [Internet] [Masters thesis]. University of Hong Kong; 2012. [cited 2020 Feb 17]. Available from: Zhang, J. [张婧]. (2012). The immunomodulatory properties of Cordyceps cicadae on resting and proliferating human T-lymphocytes. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4961803 ; http://dx.doi.org/10.5353/th_b4961803 ; http://hdl.handle.net/10722/180982.

Council of Science Editors:

Zhang J. The immunomodulatory properties of Cordyceps cicadae on resting and proliferating human T-lymphocytes. [Masters Thesis]. University of Hong Kong; 2012. Available from: Zhang, J. [张婧]. (2012). The immunomodulatory properties of Cordyceps cicadae on resting and proliferating human T-lymphocytes. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4961803 ; http://dx.doi.org/10.5353/th_b4961803 ; http://hdl.handle.net/10722/180982

Universiteit Utrecht

22. Munting, L.P. Reviewing seasonal child vaccination against influenza: An evaluation of the pros and cons.

Degree: 2015, Universiteit Utrecht

URL: http://dspace.library.uu.nl:8080/handle/1874/303162

► Influenza is an infectious, respiratory disease, which may cause symptoms in healthy individuals for several weeks. Serious complications or death may occur in the elderly… (more)

Subjects/Keywords: influenza; child vaccination; T cells

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APA (6^th Edition):

Munting, L. P. (2015). Reviewing seasonal child vaccination against influenza: An evaluation of the pros and cons. (Masters Thesis). Universiteit Utrecht. Retrieved from http://dspace.library.uu.nl:8080/handle/1874/303162

Chicago Manual of Style (16^th Edition):

Munting, L P. “Reviewing seasonal child vaccination against influenza: An evaluation of the pros and cons.” 2015. Masters Thesis, Universiteit Utrecht. Accessed February 17, 2020. http://dspace.library.uu.nl:8080/handle/1874/303162.

MLA Handbook (7^th Edition):

Munting, L P. “Reviewing seasonal child vaccination against influenza: An evaluation of the pros and cons.” 2015. Web. 17 Feb 2020.

Vancouver:

Munting LP. Reviewing seasonal child vaccination against influenza: An evaluation of the pros and cons. [Internet] [Masters thesis]. Universiteit Utrecht; 2015. [cited 2020 Feb 17]. Available from: http://dspace.library.uu.nl:8080/handle/1874/303162.

Council of Science Editors:

Munting LP. Reviewing seasonal child vaccination against influenza: An evaluation of the pros and cons. [Masters Thesis]. Universiteit Utrecht; 2015. Available from: http://dspace.library.uu.nl:8080/handle/1874/303162

University of Otago

23. Czepluch, Wenzel. Factors mediating successful oral vaccination with lipid-encapsulated Mycobacterium bovis BCG .

Degree: 2012, University of Otago

URL: http://hdl.handle.net/10523/2086

► During the course of this thesis factors mediating successful oral vaccination with lipidencapsulated Mycobacterium bovis BCG were examined. Mice were fed 2x10E07 CFU BCG encapsulated… (more)

▼ During the course of this thesis factors mediating successful oral vaccination with lipidencapsulated Mycobacterium bovis BCG were examined. Mice were fed 2x10E07 CFU BCG encapsulated into a lipid matrix to prevent destruction by the gastrointestinal tract and to allow passage through the gut epithelia. In order to trace the vaccine following oral vaccination, mice were sacrificed at various time points ranging from 6 hours to 8 weeks post vaccination, and macerated lymphatic and non-lymphatic organs plated on solid agar. Initially, BCG was distributed widely in lymphatic and non-lymphatic organs, however, BCG was cleared quickly from most organs and formed small populations of less than 500 CFU/mouse in the mesenteric and cervical lymph nodes, as well as the Peyer’s patches 8 weeks post vaccination. Immuno-histochemistry and confocal microscopy, showed that BCG was absent from the follicles, but instead resided in the T cell containing intra-follicular areas. Very rarely BCG was associated with small CD11b+ cells that did not resemble typical macrophages and lacked peroxidase activity. Instead the majority of BCG could be found forming extracellular groups of 1-4 rods. This was confirmed using cell sorting of leukocytes isolated from alimentary tract lymphatics of orally vaccinated mice and only showed a minority of BCG to be associated with CD11c+ cells. Therefore, BCG is absent from typical antigen presenting cells, but instead might reside in CD11c+CD11b+ myeloid DC. Additionally, Ziehl-Neelsen staining revealed groups of intracellular coccoid forms of BCG. These were located toward the subcapsular space of draining lymph nodes where they were associated with sub-capsular macrophages. Interestingly, cocci proved to be non-platable using solid agar but instead required resuscitation in liquid media and therefore might resemble a form of dormancy. The presence of extracellular rods and intracellular cocci in on-professional antigen presenting cells might highlight the importance of secreted factors as an antigen source promoting successful activation of the immune system. Following oral vaccination, IFN-γ producing cells almost exclusively resided in the spleen. In order to characterize these cells, splenocytes of orally vaccinated mice were isolated 6 weeks post vaccination on the basis of surface marker expression using fluorescence activated cell sorting (FACS). Antigen-specific release of IFN-γ was monitored using ELISA and ELISpot assays and IFN-γ producing T cells were characterized as T effector memory cells expressing CD44, but not CD62L and lacked the expression of mucosal homing markers such as CD103 or α4β7. In addition, Lincoplex assays revealed the production of IL-17 by splenocytes. These did not express CD4+ but rather the γδ T cell eceptor. Together these results show that antigen reservoirs of BCG present in the draining lymphatics contain small numbers of typical filamentous BCG. A larger population of coccoid forms leaves open the possibility that coccoid forms are a major source of antigen… Advisors/Committee Members: McLellan, Alexander Donald (advisor).

Subjects/Keywords: BCG vaccination; T cells DC

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

APA (6^th Edition):

Czepluch, W. (2012). Factors mediating successful oral vaccination with lipid-encapsulated Mycobacterium bovis BCG . (Doctoral Dissertation). University of Otago. Retrieved from http://hdl.handle.net/10523/2086

Chicago Manual of Style (16^th Edition):

Czepluch, Wenzel. “Factors mediating successful oral vaccination with lipid-encapsulated Mycobacterium bovis BCG .” 2012. Doctoral Dissertation, University of Otago. Accessed February 17, 2020. http://hdl.handle.net/10523/2086.

MLA Handbook (7^th Edition):

Czepluch, Wenzel. “Factors mediating successful oral vaccination with lipid-encapsulated Mycobacterium bovis BCG .” 2012. Web. 17 Feb 2020.

Vancouver:

Czepluch W. Factors mediating successful oral vaccination with lipid-encapsulated Mycobacterium bovis BCG . [Internet] [Doctoral dissertation]. University of Otago; 2012. [cited 2020 Feb 17]. Available from: http://hdl.handle.net/10523/2086.

Council of Science Editors:

Czepluch W. Factors mediating successful oral vaccination with lipid-encapsulated Mycobacterium bovis BCG . [Doctoral Dissertation]. University of Otago; 2012. Available from: http://hdl.handle.net/10523/2086

Montana Tech

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

Degree: PhD, 2013, Montana Tech

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). Montana Tech. 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, Montana Tech. Accessed February 17, 2020. https://scholarworks.umt.edu/etd/100.

MLA Handbook (7^th Edition):

Osborne, Douglas Grant. “Biological effects of trogocytosis on CD4+ T lymphocytes.” 2013. Web. 17 Feb 2020.

Vancouver:

Osborne DG. Biological effects of trogocytosis on CD4+ T lymphocytes. [Internet] [Doctoral dissertation]. Montana Tech; 2013. [cited 2020 Feb 17]. Available from: https://scholarworks.umt.edu/etd/100.

Council of Science Editors:

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

University of Manchester

25. Davies, Sian. T Cell Phenotypes in Upper Gastrointestinal Cancers.

Degree: 2016, University of Manchester

URL: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:300583

► AbstractBackground: Upper gastrointestinal adenocarcinomas are increasing in prevalence, particularly oesophageal cancer where the incidence rates have increased by over 65% in the last 30 years.… (more)

▼ AbstractBackground: Upper gastrointestinal adenocarcinomas are increasing in prevalence, particularly oesophageal cancer where the incidence rates have increased by over 65% in the last 30 years. Both adenocarcinomas are associated with very poor outcomes; the 5 year survival rate for oesophageal cancer being only 15% and gastric cancer 19%. There has been limited research into the role of the immune system in the development and treatment of upper gastrointestinal adenocarcinomas. Some studies have suggested that certain T helper subsets, including Th17 and Th22 cells, may play a role in these cancers and could therefore be a potential area of further study. However the classification of these cell types has altered over time in part due to the increased availability of marker–specific antibodies and increased power of multi-colour flow cytometry technology. Thus, the limited ability to clearly detect specific T cell subsets in earlier studies may have contributed to the contradictory roles predicted for these T helper subsets cells in the development of upper gastrointestinal malignancy. Aims: This project focuses on developing multi-colour flow cytometry panels that can accurately identify the diversity of T helper cell phenotypes and use these techniques to further explore the role these cells may have in the development and disease process of upper gastrointestinal adenocarcinomas.Methods: Blood samples from healthy donors and patients with either gastric adenocarcinoma or oesophageal adenocarcinoma would be collected and matched peripheral blood mononuclear cells (PBMC) isolated. Experiments were performed to develop an optimized flow cytometry panel that could identify the subtype populations of CD4 cells Th17 and Th22 by varying the duration of activation and the freeze / thawing of the PBMCs. Alongside this process, a flow cytometry technique was developed to optimize the identification of these populations. Once this methodological process was optimised, healthy donor PBMCs and gastric or oesophageal cancer PBMCs were analysed to determine the relative frequency of Th17 and Th22 cells within the different patient and healthy donor cellular populations. Results: The optimal activation period to identification of Th17 and Th22 cells was 16 hours. Moreover, freeze / thawing had minimal impact on the ability to identify these populations thereby facilitating the batched analysis with improved consistency in sample analysis. A flow cytometry panel of 10 flourochromes was also designed and optimised to more accurately improve identification of Th17 and Th22 by their cytokine profiles CD3+CD4+IL17+IL10-INF?- and CD3+CD4+IL22+IL17-TNF?+ respectively. To also identify the possible plastic nature of Th17 cells, further populations were defined by their cytokine profiles Th17/Treg (CD3+CD4+IL-17+IL-10+INF?-) and Th17/Th1 (CD3+CD4+IL-17+IL-10-INF?+). Analyses of these populations in healthy donor PBMCs found a significant positive correlation between the relative frequency of Th17 and Th22 cells, Th17/Th1 and Th22… Advisors/Committee Members: MANSOOR, ABDUL AW, GALLOWAY, SIMON S, Gilham, David, Mansoor, Abdul, Galloway, Simon.

Subjects/Keywords: T Cells; Upper GI Cancers

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APA (6^th Edition):

Davies, S. (2016). T Cell Phenotypes in Upper Gastrointestinal Cancers. (Doctoral Dissertation). University of Manchester. Retrieved from http://www.manchester.ac.uk/escholar/uk-ac-man-scw:300583

Chicago Manual of Style (16^th Edition):

Davies, Sian. “T Cell Phenotypes in Upper Gastrointestinal Cancers.” 2016. Doctoral Dissertation, University of Manchester. Accessed February 17, 2020. http://www.manchester.ac.uk/escholar/uk-ac-man-scw:300583.

MLA Handbook (7^th Edition):

Davies, Sian. “T Cell Phenotypes in Upper Gastrointestinal Cancers.” 2016. Web. 17 Feb 2020.

Vancouver:

Davies S. T Cell Phenotypes in Upper Gastrointestinal Cancers. [Internet] [Doctoral dissertation]. University of Manchester; 2016. [cited 2020 Feb 17]. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:300583.

Council of Science Editors:

Davies S. T Cell Phenotypes in Upper Gastrointestinal Cancers. [Doctoral Dissertation]. University of Manchester; 2016. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:300583

University of Oxford

26. Wallace, Zoë R. Application of engineered T cell receptors to investigate the failure of cytotoxic T lymphocytes to eliminate the HIV reservoir.

Degree: PhD, 2017, University of Oxford

URL: http://ora.ox.ac.uk/objects/uuid:a7b1d93d-2637-4197-b18a-726d96352043 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.740917

► HIV establishes a reservoir comprising long lived, latently infected CD4+ T cells and monocytic cells early during primary infection. This population represents a major barrier… (more)

▼ HIV establishes a reservoir comprising long lived, latently infected CD4+ T cells and monocytic cells early during primary infection. This population represents a major barrier to an HIV cure. This thesis aimed to investigate the role of the immunological synapse in the failure of cytotoxic T lymphocytes (CTLs) to eliminate the HIV reservoir and the potential for engineered bispecific Immune-mobilising monoclonal T cell receptors Against Viruses (ImmTAV) to overcome this by redirecting fully functional CD8+ T cells against viral targets. A primary cell model of latency was used to investigate the expression of HIV Gag on latently infected cells and their susceptibility to ImmTAV-mediated elimination. A subset of cells expressed low levels of Gag without spreading infection and ImmTAV-redirected healthy donor CD8+ T cells were able to eliminate up to 40% of infected cells without latency reversal. CD8+ T cells from chronic HIV infected (CHI) donors showed impaired antiviral activity even with ImmTAV redirection. To investigate this further, confocal microscopy was used to study immunological synapse formation using primary CD8+ T cells from HIV-negative and CHI donors. CD8+ T cells from CHI donors were able to form conjugates with virus-infected cells but exhibited impaired synapse maturation, indicated by reduced Zap70 localisation, delayed microtubule-organising centre polarisation and impaired perforin recruitment to the synapse. ImmTAV redirection partially overcame these defects. Finally, the impact of antiretroviral agents on T cell mitochondrial function was explored. Exposure to zidovudine increased mitochondrial reactive oxygen species production and susceptibility to apoptosis. However, there was no evidence of impaired mitophagy. These data show that defects in CD4+/CD8+ T cell synapse maturation contribute to HIV persistence but nevertheless suggest that a subset of HIV reservoir cells may be susceptible to ImmTAV-mediated elimination. The therapeutic potential of ImmTAVs may depend in part on correction of CD8+ T cell exhaustion.

Subjects/Keywords: Immunology; T cells; HIV; Reservoir

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

APA (6^th Edition):

Wallace, Z. R. (2017). Application of engineered T cell receptors to investigate the failure of cytotoxic T lymphocytes to eliminate the HIV reservoir. (Doctoral Dissertation). University of Oxford. Retrieved from http://ora.ox.ac.uk/objects/uuid:a7b1d93d-2637-4197-b18a-726d96352043 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.740917

Chicago Manual of Style (16^th Edition):

Wallace, Zoë R. “Application of engineered T cell receptors to investigate the failure of cytotoxic T lymphocytes to eliminate the HIV reservoir.” 2017. Doctoral Dissertation, University of Oxford. Accessed February 17, 2020. http://ora.ox.ac.uk/objects/uuid:a7b1d93d-2637-4197-b18a-726d96352043 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.740917.

MLA Handbook (7^th Edition):

Wallace, Zoë R. “Application of engineered T cell receptors to investigate the failure of cytotoxic T lymphocytes to eliminate the HIV reservoir.” 2017. Web. 17 Feb 2020.

Vancouver:

Wallace ZR. Application of engineered T cell receptors to investigate the failure of cytotoxic T lymphocytes to eliminate the HIV reservoir. [Internet] [Doctoral dissertation]. University of Oxford; 2017. [cited 2020 Feb 17]. Available from: http://ora.ox.ac.uk/objects/uuid:a7b1d93d-2637-4197-b18a-726d96352043 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.740917.

Council of Science Editors:

Wallace ZR. Application of engineered T cell receptors to investigate the failure of cytotoxic T lymphocytes to eliminate the HIV reservoir. [Doctoral Dissertation]. University of Oxford; 2017. Available from: http://ora.ox.ac.uk/objects/uuid:a7b1d93d-2637-4197-b18a-726d96352043 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.740917

University of Cambridge

27. Alam, Rafeah. T cell phenotyping of a mouse model of Activated PI3Kdelta syndrome.

Degree: PhD, 2019, University of Cambridge

URL: https://www.repository.cam.ac.uk/handle/1810/293595

► Activated PI3Kdelta Syndrome (APDS) is immunodeficiency caused by a heterozygous gain-of-function mutation (E1021K) in the PIK3CD gene, encoding for the p110delta catalytic subunit of phosphoinositide… (more)

Subjects/Keywords: APDS; PI3K; T cells

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

APA (6^th Edition):

Alam, R. (2019). T cell phenotyping of a mouse model of Activated PI3Kdelta syndrome. (Doctoral Dissertation). University of Cambridge. Retrieved from https://www.repository.cam.ac.uk/handle/1810/293595

Chicago Manual of Style (16^th Edition):

Alam, Rafeah. “T cell phenotyping of a mouse model of Activated PI3Kdelta syndrome.” 2019. Doctoral Dissertation, University of Cambridge. Accessed February 17, 2020. https://www.repository.cam.ac.uk/handle/1810/293595.

MLA Handbook (7^th Edition):

Alam, Rafeah. “T cell phenotyping of a mouse model of Activated PI3Kdelta syndrome.” 2019. Web. 17 Feb 2020.

Vancouver:

Alam R. T cell phenotyping of a mouse model of Activated PI3Kdelta syndrome. [Internet] [Doctoral dissertation]. University of Cambridge; 2019. [cited 2020 Feb 17]. Available from: https://www.repository.cam.ac.uk/handle/1810/293595.

Council of Science Editors:

Alam R. T cell phenotyping of a mouse model of Activated PI3Kdelta syndrome. [Doctoral Dissertation]. University of Cambridge; 2019. Available from: https://www.repository.cam.ac.uk/handle/1810/293595

University of Cambridge

28. Strege, Katharina. Identifying regulators of cytotoxic T cell function through molecular and genetic screening.

Degree: PhD, 2019, University of Cambridge

URL: https://www.repository.cam.ac.uk/handle/1810/293498https://www.repository.cam.ac.uk/bitstream/1810/293498/2/AppendixB.csv

► Cytotoxic T lymphocytes (CTL) are crucial components of the adaptive immune system that kill infected and tumourigenic cells. CTL killing requires focused secretion of cytotoxic… (more)

▼ Cytotoxic T lymphocytes (CTL) are crucial components of the adaptive immune system that kill infected and tumourigenic cells. CTL killing requires focused secretion of cytotoxic compounds from lytic granules. This process is known as degranulation. In this study, I aimed to establish the CRISPR-Cas9 gene editing technology in primary T cells and to optimise screening approaches to identify regulators of CTL killing. The first half of the thesis focuses on primary mouse CTL. The CRISPR technology was successfully optimised in CTL using Cas9-ribonucleoprotein complexes resulting in efficient CRISPR-mediated loss of target proteins. Genes encoding known mediators of CTL cytotoxicity, \it{Rab27a}, \it{Munc13-4} and \it{Prf1}, were targeted using CRISPR. The resulting samples were used to establish a flow cytometry-based assay that simultaneously measures CTL degranulation and target cell death. This assay enabled me to screen for mediators of CTL killing, while providing mechanistic insight by detecting degranulation. The screen was informed by a transcriptomic study that compared naive and effector CD8 T cells. 1803 significantly upregulated differentially expressed genes [log2(fold change)>2] were identified. Functional annotation analysis and literature research were used to select genes for the targeted CRISPR screen, which highlighted the importance of HIF-1α and NFIL3 in CTL killing. The second half of the thesis focuses on primary human CTL. The combined degranulation and killing assay was further validated using patient-derived CTL, indicating its potential as a diagnostic test. I showed that the assay is suitable for mid-sized screens using a library of 64 compounds targeting the NF-κB signalling pathway. Further opportunities for increasing the scale of this screening technique are discussed. Finally, I successfully tested CRISPR using Cas9-ribonucleoprotein complexes in the human system. Additionally, stable Cas9 expression through lentiviral transduction was explored in primary CTL and related cell lines. This has the potential to allow selection of cells expressing the CRISPR machinery, providing a cleaner experimental system and the possibility of large-scale screening approaches. In summary, the techniques established in this thesis will be valuable for studying the genetics underlying CTL killing and the combined degranulation and killing assay furthermore shows great potential for diagnostic purposes.

Subjects/Keywords: Cytotoxic T cells; CRISPR; screening

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

APA (6^th Edition):

Strege, K. (2019). Identifying regulators of cytotoxic T cell function through molecular and genetic screening. (Doctoral Dissertation). University of Cambridge. Retrieved from https://www.repository.cam.ac.uk/handle/1810/293498https://www.repository.cam.ac.uk/bitstream/1810/293498/2/AppendixB.csv

Chicago Manual of Style (16^th Edition):

Strege, Katharina. “Identifying regulators of cytotoxic T cell function through molecular and genetic screening.” 2019. Doctoral Dissertation, University of Cambridge. Accessed February 17, 2020. https://www.repository.cam.ac.uk/handle/1810/293498https://www.repository.cam.ac.uk/bitstream/1810/293498/2/AppendixB.csv.

MLA Handbook (7^th Edition):

Strege, Katharina. “Identifying regulators of cytotoxic T cell function through molecular and genetic screening.” 2019. Web. 17 Feb 2020.

Vancouver:

Strege K. Identifying regulators of cytotoxic T cell function through molecular and genetic screening. [Internet] [Doctoral dissertation]. University of Cambridge; 2019. [cited 2020 Feb 17]. Available from: https://www.repository.cam.ac.uk/handle/1810/293498https://www.repository.cam.ac.uk/bitstream/1810/293498/2/AppendixB.csv.

Council of Science Editors:

Strege K. Identifying regulators of cytotoxic T cell function through molecular and genetic screening. [Doctoral Dissertation]. University of Cambridge; 2019. Available from: https://www.repository.cam.ac.uk/handle/1810/293498https://www.repository.cam.ac.uk/bitstream/1810/293498/2/AppendixB.csv

Cornell University

29. Carter, Chavez. Role Of Itk In Th17 Mediated Inflammation Model Hypersensitivity Pneumonitis .

Degree: 2015, Cornell University

URL: http://hdl.handle.net/1813/41075

► Hypersensitivity Pneumonitis (HP) is a lung disease caused by repeated inhalation of environmental antigens leading to inflammation, tissue scarring, and some loss of lung function.… (more)

Subjects/Keywords: Itk; Hypersensitivity Pneumonitis; T cells

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

APA (6^th Edition):

Carter, C. (2015). Role Of Itk In Th17 Mediated Inflammation Model Hypersensitivity Pneumonitis . (Thesis). Cornell University. Retrieved from http://hdl.handle.net/1813/41075

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):

Carter, Chavez. “Role Of Itk In Th17 Mediated Inflammation Model Hypersensitivity Pneumonitis .” 2015. Thesis, Cornell University. Accessed February 17, 2020. http://hdl.handle.net/1813/41075.

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

MLA Handbook (7^th Edition):

Carter, Chavez. “Role Of Itk In Th17 Mediated Inflammation Model Hypersensitivity Pneumonitis .” 2015. Web. 17 Feb 2020.

Vancouver:

Carter C. Role Of Itk In Th17 Mediated Inflammation Model Hypersensitivity Pneumonitis . [Internet] [Thesis]. Cornell University; 2015. [cited 2020 Feb 17]. Available from: http://hdl.handle.net/1813/41075.

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

Council of Science Editors:

Carter C. Role Of Itk In Th17 Mediated Inflammation Model Hypersensitivity Pneumonitis . [Thesis]. Cornell University; 2015. Available from: http://hdl.handle.net/1813/41075

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

Columbia University

30. Cvetkovski, Filip. Transcriptional control of tissue-resident memory T cell generation.

Degree: 2019, Columbia University

URL: https://doi.org/10.7916/d8-n16c-b343

► Tissue-resident memory T cells (TRM) are a non-circulating subset of memory that are maintained at sites of pathogen entry and mediate optimal protection against reinfection.… (more)

▼ Tissue-resident memory T cells (TRM) are a non-circulating subset of memory that are maintained at sites of pathogen entry and mediate optimal protection against reinfection. Lung TRM can be generated in response to respiratory infection or vaccination, however, the molecular pathways involved in CD4+TRM establishment have not been defined. Here, we performed transcriptional profiling of influenza-specific lung CD4+TRM following influenza infection to identify pathways implicated in CD4+TRM generation and homeostasis. Lung CD4+TRM displayed a unique transcriptional profile distinct from spleen memory, including up-regulation of a gene network induced by the transcription factor IRF4, a known regulator of effector T cell differentiation. In addition, the gene expression profile of lung CD4+TRM was enriched in gene sets previously described in tissue-resident regulatory T cells. Up-regulation of immunomodulatory molecules such as CTLA-4, PD-1, and ICOS, suggested a potential regulatory role for CD4+TRM in tissues. Using loss-of-function genetic experiments in mice, we demonstrate that IRF4 is required for the generation of lung-localized pathogen-specific effector CD4+T cells during acute influenza infection. Influenza-specific IRF4−/− T cells failed to fully express CD44, and maintained high levels of CD62L compared to wild type, suggesting a defect in complete differentiation into lung-tropic effector T cells. This finding identifies IRF4 as an important regulator of CD4+TRM generation in response to respiratory infection. Furthermore, comparing whole transcriptome profiling of mouse and human lung memory T cell subsets, we define a lung CD4+TRM gene signature common to mice and humans. IRF4 protein was specifically up-regulated in lung CD4+TRM but not in circulating memory subsets, in both humans and mice previously infected with influenza. This result suggest that high expression of IRF4 contributes to a cross-species conserved molecular pathway of long term maintenance of CD4+TRM in the lung. Overall, our findings confirm lung CD4+TRM as a unique memory T cell subset regulated by tissue-specific transcription factors. These results have important implications in focusing future studies of tissue resident memory T cells to factors with translational potential. Importantly, by determining the lung CD4+TRM gene signature common to mice and humans, we motivate future genetic studies that could lead to the complete identification of the mechanisms of TRM maintenance in humans.

Subjects/Keywords: Immunology; T cells; Genetic transcription

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

APA (6^th Edition):

Cvetkovski, F. (2019). Transcriptional control of tissue-resident memory T cell generation. (Doctoral Dissertation). Columbia University. Retrieved from https://doi.org/10.7916/d8-n16c-b343

Chicago Manual of Style (16^th Edition):

Cvetkovski, Filip. “Transcriptional control of tissue-resident memory T cell generation.” 2019. Doctoral Dissertation, Columbia University. Accessed February 17, 2020. https://doi.org/10.7916/d8-n16c-b343.

MLA Handbook (7^th Edition):

Cvetkovski, Filip. “Transcriptional control of tissue-resident memory T cell generation.” 2019. Web. 17 Feb 2020.

Vancouver:

Cvetkovski F. Transcriptional control of tissue-resident memory T cell generation. [Internet] [Doctoral dissertation]. Columbia University; 2019. [cited 2020 Feb 17]. Available from: https://doi.org/10.7916/d8-n16c-b343.

Council of Science Editors:

Cvetkovski F. Transcriptional control of tissue-resident memory T cell generation. [Doctoral Dissertation]. Columbia University; 2019. Available from: https://doi.org/10.7916/d8-n16c-b343

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Open Access Theses and Dissertations