subject:(Immunity)

University of Georgia

1. Connor, Meghan Ashley. Role of a novel pattern recognition receptor in antibacterial innate immunity.

Degree: MS, Infectious Diseases, 2008, University of Georgia

URL: http://purl.galileo.usg.edu/uga_etd/connor_meghan_a_200805_ms

► Teleosts are an evolutionarily appropriate model for studying immunology. The innate immune system of fish is the principal defense mechanism. The acquired immune system is… (more)

Subjects/Keywords: Innate Immunity

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APA (6^th Edition):

Connor, M. A. (2008). Role of a novel pattern recognition receptor in antibacterial innate immunity. (Masters Thesis). University of Georgia. Retrieved from http://purl.galileo.usg.edu/uga_etd/connor_meghan_a_200805_ms

Chicago Manual of Style (16^th Edition):

Connor, Meghan Ashley. “Role of a novel pattern recognition receptor in antibacterial innate immunity.” 2008. Masters Thesis, University of Georgia. Accessed February 25, 2020. http://purl.galileo.usg.edu/uga_etd/connor_meghan_a_200805_ms.

MLA Handbook (7^th Edition):

Connor, Meghan Ashley. “Role of a novel pattern recognition receptor in antibacterial innate immunity.” 2008. Web. 25 Feb 2020.

Vancouver:

Connor MA. Role of a novel pattern recognition receptor in antibacterial innate immunity. [Internet] [Masters thesis]. University of Georgia; 2008. [cited 2020 Feb 25]. Available from: http://purl.galileo.usg.edu/uga_etd/connor_meghan_a_200805_ms.

Council of Science Editors:

Connor MA. Role of a novel pattern recognition receptor in antibacterial innate immunity. [Masters Thesis]. University of Georgia; 2008. Available from: http://purl.galileo.usg.edu/uga_etd/connor_meghan_a_200805_ms

University of Georgia

2. Thoetkiattikul, Honglada. Expression and functional studies of the Microplitis demolitor bracovirus IkB-like gene family.

Degree: PhD, Entomology, 2006, University of Georgia

URL: http://purl.galileo.usg.edu/uga_etd/thoetkiattikul_honglada_200608_phd

► Complex signaling pathways regulate the innate immune system of insects, with NF-kBtranscription factors playing a central role in the activation of antimicrobial peptides and otherimmune… (more)

Subjects/Keywords: Immunity

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APA (6^th Edition):

Thoetkiattikul, H. (2006). Expression and functional studies of the Microplitis demolitor bracovirus IkB-like gene family. (Doctoral Dissertation). University of Georgia. Retrieved from http://purl.galileo.usg.edu/uga_etd/thoetkiattikul_honglada_200608_phd

Chicago Manual of Style (16^th Edition):

Thoetkiattikul, Honglada. “Expression and functional studies of the Microplitis demolitor bracovirus IkB-like gene family.” 2006. Doctoral Dissertation, University of Georgia. Accessed February 25, 2020. http://purl.galileo.usg.edu/uga_etd/thoetkiattikul_honglada_200608_phd.

MLA Handbook (7^th Edition):

Thoetkiattikul, Honglada. “Expression and functional studies of the Microplitis demolitor bracovirus IkB-like gene family.” 2006. Web. 25 Feb 2020.

Vancouver:

Thoetkiattikul H. Expression and functional studies of the Microplitis demolitor bracovirus IkB-like gene family. [Internet] [Doctoral dissertation]. University of Georgia; 2006. [cited 2020 Feb 25]. Available from: http://purl.galileo.usg.edu/uga_etd/thoetkiattikul_honglada_200608_phd.

Council of Science Editors:

Thoetkiattikul H. Expression and functional studies of the Microplitis demolitor bracovirus IkB-like gene family. [Doctoral Dissertation]. University of Georgia; 2006. Available from: http://purl.galileo.usg.edu/uga_etd/thoetkiattikul_honglada_200608_phd

Texas A&M University

3. Shen, Shixue. Differential gene expression in innate immunity between commercial broilers and layers.

Degree: 2009, Texas A&M University

URL: http://hdl.handle.net/1969.1/ETD-TAMU-1848

► Tremendous improvements have been achieved in growth rates and feed efficiency in commercial broiler birds. However, fast growth broilers generally show weak immune competence and… (more)

▼ Tremendous improvements have been achieved in growth rates and feed efficiency in commercial broiler birds. However, fast growth broilers generally show weak immune competence and disease resistance. Innate immunity is the first line of defense providing immediate killing effects to a broad range of infectious pathogens and limiting infections to a minimum at an early stage before the activation of more specific adaptive immunity. Acute phase proteins (APPs), defensins and Toll-like receptors (TLRs) are all important innate immune molecules functioning from recognition to killing the foreign microbes. Tibial dyschondroplasia (TD) is one chicken disease associated with rapid growth in broilers. The objective of this research was to study the differential expression of innate immune related genes in liver and spleen tissues between commercial broilers and layers with the stimulation of lipopolysaccharide (LPS). Also, this study investigated mechanisms involved in the pathogenesis of TD at molecular levels. This study first identified and annotated nineteen new chicken APPs genes from the chicken genome draft with bioinformatics tools. Using a relative quantitative real-time RT-PCR method, the expression levels of all thirty-one APPs, thirteen defensins and eight TLRs genes were systemically investigated at the transcriptional level at three time points (0-, 3-, 8-hour) with the challenge of LPS. This study showed that broiler birds generally expressed significantly lower levels of all three families of innate immune related genes than layers and the inductive extent of these genes are generally smaller in broilers too. Close investigation of some important signaling transcription factors (NF-kB and IRF-3) and cytokine (IL-6) also reached the same conclusion. This study revealed that the inadequate expression of deiodinase type 2 (DIO2) contributed to the pathogenesis of TD in rapid growth broilers. All of the experimental results solidly validate the hypothesis that a compromised innate immune response or weak disease resistence is associated with fast growth broiler birds. Advisors/Committee Members: Caldwell, David J. (advisor), Zhu, James J. (advisor), Berghman, Luc R. (committee member), Chen, Z. Jeffrey (committee member).

Subjects/Keywords: chicken; immunity

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APA (6^th Edition):

Shen, S. (2009). Differential gene expression in innate immunity between commercial broilers and layers. (Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/ETD-TAMU-1848

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):

Shen, Shixue. “Differential gene expression in innate immunity between commercial broilers and layers.” 2009. Thesis, Texas A&M University. Accessed February 25, 2020. http://hdl.handle.net/1969.1/ETD-TAMU-1848.

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

MLA Handbook (7^th Edition):

Shen, Shixue. “Differential gene expression in innate immunity between commercial broilers and layers.” 2009. Web. 25 Feb 2020.

Vancouver:

Shen S. Differential gene expression in innate immunity between commercial broilers and layers. [Internet] [Thesis]. Texas A&M University; 2009. [cited 2020 Feb 25]. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-1848.

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

Council of Science Editors:

Shen S. Differential gene expression in innate immunity between commercial broilers and layers. [Thesis]. Texas A&M University; 2009. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-1848

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

4. Torres, Celia Aurora Tiglao. DNA Immunization: Role of Target Site, Bone Marrow-Derived Cells and Secretion of Antigen in the Initiation of Immune Responses: A Dissertation.

Degree: Graduate School of Biomedical Sciences, Department of Molecular Genetics and Microbiology, 1998, U of Massachusetts : Med

URL: http://escholarship.umassmed.edu/gsbs_diss/293

► DNA immunization, or the use of antigen-expressing DNAs to raise immune responses, represents a novel approach to the study and manipulation of immune responses.… (more)

▼ DNA immunization, or the use of antigen-expressing DNAs to raise immune responses, represents a novel approach to the study and manipulation of immune responses. In this dissertation, we examine the role of antigen expression at the target site, the role of antigen presentation by bone marrow-derived cells, and the effect of secretion of antigen on DNA-raised responses in mice. Immunizations were conducted using either gene gun delivery of DNA to the epidermis or intramuscular (i.m.) saline injections. To examine the role of antigen expression at the target site, we excised target sites at different time points following immunization. We immunized with plasmid DNA expressing three different forms of antigens: influenza hemagglutinin H1, human growth hormone and influenza nucleoprotein NP (membrane-bound, secreted and intracellular, respectively). We hypothesized that antigen expression at the target site would be essential in initiating immune responses. We demonstrate here that the target site plays different roles in gene gun and i.m. immunizations. We found that the skin target site played an essential role in eliciting maximal antibody and cytotoxic T lymphocyte (CTL) responses by gene gun immunization, although low-level responses can be raised independent of the target site. In contrast, the muscle target site was not essential for eliciting maximal immune responses following i.m. immunization. We suggest that gene gun immunization results in transfection of keratinocytes and bone marrow-derived Langerhans cells at the target site, and these cells together initiate maximal responses. In i.m. immunizations, on the other hand, nonmuscle cells at distal sites, perhaps bone marrow-derived cells in lymphoid tissues, become transfected and are sufficient for initiation of maximal responses. We also examined the role of antigen presentation by bone marrow-derived cells in initiation of CTL responses to influenza NP following gene gun and i.m. immunization. We hypothesized that antigen presentation by bone marrow-derived cells would be involved in initiation of CTL responses. To test this hypothesis, irradiated F1 mice of MHC class I H-2^bxd haplotype were reconstituted with bone marrow from either H-2^b or H-2^d donors, creating two sets of bone marrow chimeric mice (H-2^b → H-2^bxd and H-2^d → H-2^bxd, respectively). We immunized the two sets of bone marrow chimeric mice and determined the MHC haplotype restriction of the induced CTL responses using H-2^b- or H-2^d-restricted peptides of NP. We found that the CTL responses initiated following gene gun and i.m. immunization were restricted to the haplotype of the bone marrow donor. In H-2^b→ H-2^bxd chimeric mice, CTL responses were restricted to H-2^b, while in H-2^d→ H-2^bxd chimeric mice, CTL responses were restricted to H-2^d. Thus, antigen presentation by bone marrow-derived cells, and not by skin…

Subjects/Keywords: Immunity

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APA (6^th Edition):

Torres, C. A. T. (1998). DNA Immunization: Role of Target Site, Bone Marrow-Derived Cells and Secretion of Antigen in the Initiation of Immune Responses: A Dissertation. (Doctoral Dissertation). U of Massachusetts : Med. Retrieved from http://escholarship.umassmed.edu/gsbs_diss/293

Chicago Manual of Style (16^th Edition):

Torres, Celia Aurora Tiglao. “DNA Immunization: Role of Target Site, Bone Marrow-Derived Cells and Secretion of Antigen in the Initiation of Immune Responses: A Dissertation.” 1998. Doctoral Dissertation, U of Massachusetts : Med. Accessed February 25, 2020. http://escholarship.umassmed.edu/gsbs_diss/293.

MLA Handbook (7^th Edition):

Torres, Celia Aurora Tiglao. “DNA Immunization: Role of Target Site, Bone Marrow-Derived Cells and Secretion of Antigen in the Initiation of Immune Responses: A Dissertation.” 1998. Web. 25 Feb 2020.

Vancouver:

Torres CAT. DNA Immunization: Role of Target Site, Bone Marrow-Derived Cells and Secretion of Antigen in the Initiation of Immune Responses: A Dissertation. [Internet] [Doctoral dissertation]. U of Massachusetts : Med; 1998. [cited 2020 Feb 25]. Available from: http://escholarship.umassmed.edu/gsbs_diss/293.

Council of Science Editors:

Torres CAT. DNA Immunization: Role of Target Site, Bone Marrow-Derived Cells and Secretion of Antigen in the Initiation of Immune Responses: A Dissertation. [Doctoral Dissertation]. U of Massachusetts : Med; 1998. Available from: http://escholarship.umassmed.edu/gsbs_diss/293

5. Davidovics, Sarah A. Low-grade inflammation, immune capacity, and cancer.

Degree: 2014, Johns Hopkins University

URL: http://jhir.library.jhu.edu/handle/1774.2/37166

► Inflammation is a well-established etiological factor in carcinogenesis. The immune system may also have the capacity to identify and clear malignant cells in a process… (more)

▼ Inflammation is a well-established etiological factor in carcinogenesis. The immune system may also have the capacity to identify and clear malignant cells in a process known as tumor immunosurveillance. The objective of this dissertation is to examine these roles of host immunity in carcinogenesis in immunocompetent adults. Specifically, we quantified the risk of cancer incidence and mortality by circulating, pre-diagnostic levels of the white blood cell (WBC) subtypes, neutrophils, lymphocytes, monocytes, eosinophils, and basophils, and cytomegalovirus (CMV) IgG titer in two longitudinal cohorts, the Atherosclerosis Risk in Communities (ARIC), 1987-2008, and the third National Health and Nutrition Examination Survey (NHANES III), 1988-2011. Multivariate Cox analyses were used to estimate the hazard ratios (HR) and 95% confidence intervals (CI) of cancer incidence and mortality by levels of immune markers. High neutrophil count was associated with an increased risk of total (HR: 1.11, 95% CI: 1.00, 1.25) and lung (HR: 1.59, 95% CI: 1.12, 2.26) cancer incidence, and total (HR: 1.44, 95% CI: 1.22, 1.72), lung (HR: 1.66, 95% CI: 1.18, 2.33) and breast (HR: 2.09, 95% CI: 1.10, 3.97) cancer mortality. Among men, high lymphocyte count was associated with a reduced risk of cancer incidence, after excluding prostate cancer (HR: 0.75, 95% CI: 0.62, 0.91), and an increased risk of prostate cancer incidence (HR: 1.31, 95% CI: 1.03, 1.66). Among women, lymphocyte count was positively associated with cancer mortality (HR: 1.40, 95% CI: 1.07, 1.82). The presence of basophils in circulation was associated with a reduced risk of cancer incidence (HR: 0.93, 95% CI: 0.85, 1.01) and mortality (HR: 0.87, 95% CI: 0.76, 1.00). Adjustment for the other WBC subtypes did not appreciably alter these estimates. No associations were found for monocyte or eosinophil counts. Lastly, high CMV IgG antibody titer was associated with increased cancer mortality in black CMV seropositive persons (HR: 1.38, 95% CI: 1.02, 1.89), while no association was present in whites or Mexican Americans. Our findings of an association between circulating pre-diagnostic levels of neutrophils, lymphocytes, basophils, and CMV IgG and cancer incidence and mortality support a role for low-grade inflammation and subclinical immune suppression in carcinogenesis. Advisors/Committee Members: Wang, Mei-Cheng (advisor).

Subjects/Keywords: cancer; immunity

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APA (6^th Edition):

Davidovics, S. A. (2014). Low-grade inflammation, immune capacity, and cancer. (Thesis). Johns Hopkins University. Retrieved from http://jhir.library.jhu.edu/handle/1774.2/37166

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):

Davidovics, Sarah A. “Low-grade inflammation, immune capacity, and cancer.” 2014. Thesis, Johns Hopkins University. Accessed February 25, 2020. http://jhir.library.jhu.edu/handle/1774.2/37166.

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

MLA Handbook (7^th Edition):

Davidovics, Sarah A. “Low-grade inflammation, immune capacity, and cancer.” 2014. Web. 25 Feb 2020.

Vancouver:

Davidovics SA. Low-grade inflammation, immune capacity, and cancer. [Internet] [Thesis]. Johns Hopkins University; 2014. [cited 2020 Feb 25]. Available from: http://jhir.library.jhu.edu/handle/1774.2/37166.

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

Council of Science Editors:

Davidovics SA. Low-grade inflammation, immune capacity, and cancer. [Thesis]. Johns Hopkins University; 2014. Available from: http://jhir.library.jhu.edu/handle/1774.2/37166

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

6. Cheng, Cheng. Genetic and Biochemical Analysis of Innate Immunity in Arabidopsis thaliana.

Degree: 2013, Texas Digital Library

URL: http://hdl.handle.net/1969; http://hdl.handle.net/2249.1/66710

► Perception of evolutionarily conserved pathogen-associated molecular patterns (PAMPs) elicits rapid and profound transcriptional reprogramming in hosts and activates defense to pathogen attack. The molecular signaling… (more)

▼ Perception of evolutionarily conserved pathogen-associated molecular patterns (PAMPs) elicits rapid and profound transcriptional reprogramming in hosts and activates defense to pathogen attack. The molecular signaling networks underlying this plant pattern-triggered immunity (PTI) remain fragmented. We identified a series of mutants with altered pFRK1::LUC activity were identified and named as Arabidopsis genes governing immune gene expression (aggie) through forward genetic screening. Map-based cloning identified Aggie1 as encoding Arabidopsis C-terminal domain (CTD) phosphatase-like 3 (CPL3), a homolog of yeast FCP1 phosphatase that dephosphorylates the CTD of RNA polymerase II (RNAPII) during the transcription cycle. MAMP perception induced a rapid and transient CTD phosphorylation in Arabidopsis, underlying the modulation of CTD phosphorylation dynamics controlling plant immune responsive gene expression. Aggie1/CPL3 specifically dephosphorylated Ser2 of the CTD in vivo and in vitro and preferentially interacted with phosphorylated CTD. Transcriptional analysis indicates that cpl3 showed overall enhanced flg22-mediated transcription responses. Thus, Aggie1 negatively regulates immune responsive gene expression essential for suppression of pathogen growth by modulating the phosphorylation status of RNAPII CTD. Cyclin-dependent kinases C (CDKC) functions as RNAPII kinases. Interestingly, we also found the silencing of cdkc1 and cdkc2 in wild type reduced flg22-mediated transcription responses and the plants were more susceptible to Pseudomonas syringae DC3000, suggesting their positive role in PAMP-triggered immunity. Temperature fluctuation is a key determinant for microbial invasion into the host and for host evasion of the microbe. In contrast to mammals that maintain constant body temperature, plant internal temperature oscillates on a daily basis. It remains elusive how plants operate inducible defenses in response to temperature fluctuation. We report that ambient temperature changes lead to pronounced shifts of two distinct plant immune responses: pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) and effector-triggered immunity (ETI). Plants preferentially activate ETI signaling at relatively lower temperatures (10~23???C), whereas they switch to PTI signaling at moderately elevated temperatures (23~32???C). The Arabidopsis arp6 and hta9hta11 mutants, phenocopying plants grown at the elevated temperatures, exhibit enhanced PTI and yet reduced ETI responses. As the secretion of bacterial effectors favors low temperatures whereas bacteria multiply vigorously at elevated temperatures accompanied with increased MAMP production, our findings suggest that temperature oscillation might have driven dynamic co-evolution of distinct plant immune signaling responding to pathogen physiological changes. Advisors/Committee Members: He, Ping (advisor).

Subjects/Keywords: Plant immunity

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APA (6^th Edition):

Cheng, C. (2013). Genetic and Biochemical Analysis of Innate Immunity in Arabidopsis thaliana. (Thesis). Texas Digital Library. Retrieved from http://hdl.handle.net/1969; http://hdl.handle.net/2249.1/66710

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):

Cheng, Cheng. “Genetic and Biochemical Analysis of Innate Immunity in Arabidopsis thaliana.” 2013. Thesis, Texas Digital Library. Accessed February 25, 2020. http://hdl.handle.net/1969; http://hdl.handle.net/2249.1/66710.

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

MLA Handbook (7^th Edition):

Cheng, Cheng. “Genetic and Biochemical Analysis of Innate Immunity in Arabidopsis thaliana.” 2013. Web. 25 Feb 2020.

Vancouver:

Cheng C. Genetic and Biochemical Analysis of Innate Immunity in Arabidopsis thaliana. [Internet] [Thesis]. Texas Digital Library; 2013. [cited 2020 Feb 25]. Available from: http://hdl.handle.net/1969; http://hdl.handle.net/2249.1/66710.

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

Council of Science Editors:

Cheng C. Genetic and Biochemical Analysis of Innate Immunity in Arabidopsis thaliana. [Thesis]. Texas Digital Library; 2013. Available from: http://hdl.handle.net/1969; http://hdl.handle.net/2249.1/66710

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

7. Biron, Bethany. The Role of Peptidyl arginine deiminase, type IV (PAD4) in the Pathology of Shock/Sepsis.

Degree: Pathobiology, 2017, Brown University

URL: https://repository.library.brown.edu/studio/item/bdr:733274/

► Sepsis is a life threatening condition that elicits a dysregulated and damaging immune response, which in turn leads to tissue damage and Multiple Organ Dysfunction… (more)

▼ Sepsis is a life threatening condition that elicits a dysregulated and damaging immune response, which in turn leads to tissue damage and Multiple Organ Dysfunction (MOD). Critically ill patients that have suffered from trauma, complex surgery, gastrointestinal bleeding, obstetrical bleeding, etc., have an increased risk of developing sepsis, which may progress to Acute Respiratory Distress Syndrome (ARDS), leading in turn to an increase in mortality. Neutrophils are thought to play a role in the immune dysfunction seen in both shock and sepsis, and have been implicated in causing bystander tissue damage and organ dysfunction. Neutrophil extracellular traps (NETs) are large webs of decondensed chromatin coated with antimicrobial proteins that are released into the extracellular space. They serve as a novel effector function, regulated by the enzyme Peptidyl arginine deiminase, type IV (PAD4). NETs have been identified as an important aspect of innate immunity, but have also been linked to excessive inflammation and tissue damage. Their role in sepsis and shock/sepsis, however, is poorly understood. This dissertation examines how PAD4 (an enzyme central to NET formation) plays a role in the pathology of sepsis. It also examines whether a predispositional insult, such as severe shock antecedent to septic challenge, is affected this enzyme. Here we demonstrate that inhibition of PAD4 reduces mortality seen in a mouse polymicrobial sepsis model (CLP), as well as in a mouse model of hemorrhagic shock and sepsis (Hem/CLP). Clinically we showed that there is evidence of increased NET activity in septic patients. Together, this implies that PAD4-mediated NET formation contributes to the morbidity and mortality associated with sepsis and shock/sepsis, and that PAD4 merits further exploration as a possible therapeutic target against the damaging pro-inflammatory response seen in polymicrobial sepsis and indirect ARDS. Advisors/Committee Members: Ayala, Alfred (Advisor), Reichner, Jonathan (Reader), Lefort, Craig (Reader), Heffernan, Daithi (Reader), Levy, Bruce (Reader).

Subjects/Keywords: Cellular immunity

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APA (6^th Edition):

Biron, B. (2017). The Role of Peptidyl arginine deiminase, type IV (PAD4) in the Pathology of Shock/Sepsis. (Thesis). Brown University. Retrieved from https://repository.library.brown.edu/studio/item/bdr:733274/

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):

Biron, Bethany. “The Role of Peptidyl arginine deiminase, type IV (PAD4) in the Pathology of Shock/Sepsis.” 2017. Thesis, Brown University. Accessed February 25, 2020. https://repository.library.brown.edu/studio/item/bdr:733274/.

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

MLA Handbook (7^th Edition):

Biron, Bethany. “The Role of Peptidyl arginine deiminase, type IV (PAD4) in the Pathology of Shock/Sepsis.” 2017. Web. 25 Feb 2020.

Vancouver:

Biron B. The Role of Peptidyl arginine deiminase, type IV (PAD4) in the Pathology of Shock/Sepsis. [Internet] [Thesis]. Brown University; 2017. [cited 2020 Feb 25]. Available from: https://repository.library.brown.edu/studio/item/bdr:733274/.

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

Council of Science Editors:

Biron B. The Role of Peptidyl arginine deiminase, type IV (PAD4) in the Pathology of Shock/Sepsis. [Thesis]. Brown University; 2017. Available from: https://repository.library.brown.edu/studio/item/bdr:733274/

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

Oregon State University

8. Thompson, William Carl. The effects of actinomycin D on the primary and secondary immune responses induced in vitro.

Degree: PhD, Biochemistry and Biophysics, 1970, Oregon State University

URL: http://hdl.handle.net/1957/45640

► In order to assess the importance of RNA synthesis in the induction and antibody-producing phases of immune responses, actinomycin D was used to inhibit the… (more)

▼ In order to assess the importance of RNA synthesis in the induction and antibody-producing phases of immune responses, actinomycin D was used to inhibit the primary and secondary in vitro immune responses of mouse spleen cells against heterologous erythrocytes. The presence of actinomycin D (0.1 or 0.125 μg /ml) throughout the entire four day culture period inhibited the development of plaque-forming cells (PFCs) in both primary and secondary responses by more than 99%. The same drug concentration, if added after 1, 2, or 3 days of culture, inhibited the number of PFCs on the fourth day by 81-99%. Utilizing cultures of spleen cells from mice already undergoing a secondary immune response, no stimulation of the PFC number upon a 24 hour treatment with actinomycin D (1.25 μg /ml) was found, unlike the observation of Harris (J. Experimental Medicine 127:675, 1968), with a similar system of cultured rabbit spleen cells. The treatment of these mouse spleen suspensions for 24 hours with actinomycin D (1.25 μg /ml) usually brought about a 90-95% decrease in the number of PFCs. For both the primary and secondary in vitro immune responses the sensitivity to actinomycin D treatment throughout the culture period was determined, A drug concentration of 10⁻³ μg/ml caused no inhibition in either type of response, but rather caused some stimulation of PFC numbers by the end of the fourth day of culture, The secondary response was inhibited by 43% and 98% by actinomycin D concentrations of 3x10⁻³ and 10⁻² μg /ml respectively, The primary response was inhibited by 95% and 99% by actinomycin D concentrations of 3x10⁻³ and 10⁻² μg /ml respectively, This sensitivity of the entire response is much greater than that reported by Uyeki and Llacer (Biochemical Pharmacology 18:948, 1969) for actinomycin D additions at a later stage of the response, The spleen cell suspension was separated into a macrophagerich fraction and a lymphocyte-rich fraction. Treatment of the macrophage population for one hour with actinomycin D (0.1 μg /ml), either during or before the addition of antigen, inhibited by 95% the immune response which resulted following removal of the drug and addition of the lymphocyte-rich population to reconstitute the original cell suspension. The results are discussed with respect to the possible events occurring during the response which would account for the observed sensitivity to actinomycin D. A suggestion is made that the extremely high sensitivity of the early phases of the immune response may be due to the need for synthesis of some very large RNA molecule. Advisors/Committee Members: Newburgh, Robert W. (advisor).

Subjects/Keywords: Immunity

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

APA (6^th Edition):

Thompson, W. C. (1970). The effects of actinomycin D on the primary and secondary immune responses induced in vitro. (Doctoral Dissertation). Oregon State University. Retrieved from http://hdl.handle.net/1957/45640

Chicago Manual of Style (16^th Edition):

Thompson, William Carl. “The effects of actinomycin D on the primary and secondary immune responses induced in vitro.” 1970. Doctoral Dissertation, Oregon State University. Accessed February 25, 2020. http://hdl.handle.net/1957/45640.

MLA Handbook (7^th Edition):

Thompson, William Carl. “The effects of actinomycin D on the primary and secondary immune responses induced in vitro.” 1970. Web. 25 Feb 2020.

Vancouver:

Thompson WC. The effects of actinomycin D on the primary and secondary immune responses induced in vitro. [Internet] [Doctoral dissertation]. Oregon State University; 1970. [cited 2020 Feb 25]. Available from: http://hdl.handle.net/1957/45640.

Council of Science Editors:

Thompson WC. The effects of actinomycin D on the primary and secondary immune responses induced in vitro. [Doctoral Dissertation]. Oregon State University; 1970. Available from: http://hdl.handle.net/1957/45640

Michigan State University

9. Moorhead, John W. A study of experimental conditions affecting the secondary immune response in vitro.

Degree: MS, Dept. of Microbiology and Public Health, 1966, Michigan State University

URL: http://etd.lib.msu.edu/islandora/object/etd:14058

Subjects/Keywords: Immunity

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

APA (6^th Edition):

Moorhead, J. W. (1966). A study of experimental conditions affecting the secondary immune response in vitro. (Masters Thesis). Michigan State University. Retrieved from http://etd.lib.msu.edu/islandora/object/etd:14058

Chicago Manual of Style (16^th Edition):

Moorhead, John W. “A study of experimental conditions affecting the secondary immune response in vitro.” 1966. Masters Thesis, Michigan State University. Accessed February 25, 2020. http://etd.lib.msu.edu/islandora/object/etd:14058.

MLA Handbook (7^th Edition):

Moorhead, John W. “A study of experimental conditions affecting the secondary immune response in vitro.” 1966. Web. 25 Feb 2020.

Vancouver:

Moorhead JW. A study of experimental conditions affecting the secondary immune response in vitro. [Internet] [Masters thesis]. Michigan State University; 1966. [cited 2020 Feb 25]. Available from: http://etd.lib.msu.edu/islandora/object/etd:14058.

Council of Science Editors:

Moorhead JW. A study of experimental conditions affecting the secondary immune response in vitro. [Masters Thesis]. Michigan State University; 1966. Available from: http://etd.lib.msu.edu/islandora/object/etd:14058

Baylor University

10. Chung, Cheng-Han, 1982-. The chromatin accessibility signature of aging in human blood leukocytes stem from CD8+ T cells.

Degree: PhD, Baylor University. Institute of Biomedical Studies., 2017, Baylor University

URL: http://hdl.handle.net/2104/10165

► Human aging is linked to changes in immune function that contribute to decreased responses to pathogens and increased systemic inflammation. Human aging is also associated… (more)

▼ Human aging is linked to changes in immune function that contribute to decreased responses to pathogens and increased systemic inflammation. Human aging is also associated with profound epigenetic changes across cell types and tissues. How these changes affect the aging –associated decline of the immune system is unknown. The Assay for Transposase Accessible Chromatin with sequencing technology (ATAC-seq) allowed us to study, at a system biology level, the open chromatin landscapes of human peripheral blood mononuclear cells (PBMCs), monocytes, purified B and T cell subsets from healthy young and healthy elderly individuals. We captured aging-associated epigenomic remodeling in PBMCs consisting of (1) systematic chromatin closing at promoters and enhancers targeting the T cell signaling and development and (2) chromatin opening, mostly at quiescent and repressed sites associated with cytotoxicity. Transcriptome profiling of the same individuals revealed gene expression changes concordant with epigenomic changes. Analysis of naïve and memory CD4+ and CD8+ T cell subsets demonstrated that the epigenomic signature of aging in PBMCs arises mostly from memory CD8+ T cells, indicating that aging differentially affects T cell epigenomes in a subset-specific manner. This study provides the first systems-level description of chromatin accessibility changes associated with immune aging in human PBMCs and T cell subsets. It revealed in PBMCs significant chromatin closing at promoters and enhancers, including at the IL7R locus and the IL-7 signaling pathway. Our study revealed individual-level variability in aging-associated chromatin remodeling and provided a systematic and modular tool for assessing deviations from chronological age. The open chromatin profiling of sorted T cell subsets, concluded that the chromatin “aging signature” captured in PBMCs, mostly stems from memory CD8+ T cells. The combined ATAC-seq/RNA-seq analyses uncovered epigenetic changes poised for expression changes and active noncoding elements (e.g., enhancers), both of which will be essential for understanding the regulatory mechanisms underlying immunosenescence. Nevertheless, ATAC-seq based open chromatin profiling is a straightforward approach to identify functional genomic regulatory regions, master regulators, and gene regulatory networks controlling complex in vivo processes. In our lab, ATAC-seq is utilized to understand the epigenetics differences in different immune cells and diseases. Advisors/Committee Members: Banchereau, Jacques. (advisor).

Subjects/Keywords: Aging. Immunity.

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APA (6^th Edition):

Chung, Cheng-Han, 1. (2017). The chromatin accessibility signature of aging in human blood leukocytes stem from CD8+ T cells. (Doctoral Dissertation). Baylor University. Retrieved from http://hdl.handle.net/2104/10165

Chicago Manual of Style (16^th Edition):

Chung, Cheng-Han, 1982-. “The chromatin accessibility signature of aging in human blood leukocytes stem from CD8+ T cells.” 2017. Doctoral Dissertation, Baylor University. Accessed February 25, 2020. http://hdl.handle.net/2104/10165.

MLA Handbook (7^th Edition):

Chung, Cheng-Han, 1982-. “The chromatin accessibility signature of aging in human blood leukocytes stem from CD8+ T cells.” 2017. Web. 25 Feb 2020.

Vancouver:

Chung, Cheng-Han 1. The chromatin accessibility signature of aging in human blood leukocytes stem from CD8+ T cells. [Internet] [Doctoral dissertation]. Baylor University; 2017. [cited 2020 Feb 25]. Available from: http://hdl.handle.net/2104/10165.

Council of Science Editors:

Chung, Cheng-Han 1. The chromatin accessibility signature of aging in human blood leukocytes stem from CD8+ T cells. [Doctoral Dissertation]. Baylor University; 2017. Available from: http://hdl.handle.net/2104/10165

University of New Mexico

11. Sepahi, Ali. From olfaction to immunity: Characterization of nasal immunity in bony fish.

Degree: UNM Biology Department, 2018, University of New Mexico

URL: https://digitalrepository.unm.edu/biol_etds/277

► The olfactory system is a common route pathogen entry in vertebrates. As a consequence, the nasopharynx-associated lymphoid tissue (NALT) needs to rapidly clear infections… (more)

▼ The olfactory system is a common route pathogen entry in vertebrates. As a consequence, the nasopharynx-associated lymphoid tissue (NALT) needs to rapidly clear infections without compromising the sense of olfaction. NALT is present in teleost fish but its cellular and molecular mechanisms of action have not been investigated to this date. This dissertation focuses on three aims: 1. investigating the role of CCL19-like as a primordial chemokine in vertebrate nasal immunity, 2. determining the presence of tissue microenvironments within the olfactory organ (OO) of rainbow trout, and 3. understanding the immune contributions of olfactory sensory neurons (OSNs) in teleosts against viruses. In aim 1, we report six isoforms of CCL19-like chemokine in salmonids such as CK12. CK12 is mainly expressed in mucosal tissues and plays an important role in antiviral immunity. Although recombinant protein CK12 is not chemotactic in vitro, it induces infiltration of APCs and CD8⁺ T cells into OO of rainbow trout in vivo. In aim 2, we demonstrate the presence of two different microenvironments (mucosal tip and neuroepithelial) in the OO of rainbow trout. The tip of the epithelium harbors clusters of CD8α⁺ cells whereas few numbers are found in the neuroepithelium. CD8a⁺ cell localization corresponds with a higher expression of chemokine and chemokine receptors in the tip versus the neuroepithelial side. We report that cell proliferation in response to viral nasal delivery occurs mainly at the tip. In aim 3, we unravel for the first time a new function for OSNs by which nasal rhadboviruses induce apoptosis in crypt neurons, a type of OSN, in rainbow trout via the interaction of viral G glycoprotein and the neuron TrkA receptor. CD8α⁺ T cells infiltrate to the OO within minutes of nasal viral delivery and this response was abrogated when TrkA was blocked. Infiltrating CD8α⁺ T cells originated from the microvasculature surrounding the olfactory bulb (OB) and not the periphery. In conclusion, this dissertation provides the first tissue, cellular and molecular characterization of teleost NALT and reveals a novel function of vertebrate OSNs in eliciting rapid nasal anti-viral immune responses in the OO and OB. Advisors/Committee Members: Dr. Irene Salinas, Dr. Coenraad Adema, Dr. Judy Cannon, Dr. Jacques Robert.

Subjects/Keywords: Immunity; nasal; sensory neurons; teleost; Biology; Immunity

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APA (6^th Edition):

Sepahi, A. (2018). From olfaction to immunity: Characterization of nasal immunity in bony fish. (Doctoral Dissertation). University of New Mexico. Retrieved from https://digitalrepository.unm.edu/biol_etds/277

Chicago Manual of Style (16^th Edition):

Sepahi, Ali. “From olfaction to immunity: Characterization of nasal immunity in bony fish.” 2018. Doctoral Dissertation, University of New Mexico. Accessed February 25, 2020. https://digitalrepository.unm.edu/biol_etds/277.

MLA Handbook (7^th Edition):

Sepahi, Ali. “From olfaction to immunity: Characterization of nasal immunity in bony fish.” 2018. Web. 25 Feb 2020.

Vancouver:

Sepahi A. From olfaction to immunity: Characterization of nasal immunity in bony fish. [Internet] [Doctoral dissertation]. University of New Mexico; 2018. [cited 2020 Feb 25]. Available from: https://digitalrepository.unm.edu/biol_etds/277.

Council of Science Editors:

Sepahi A. From olfaction to immunity: Characterization of nasal immunity in bony fish. [Doctoral Dissertation]. University of New Mexico; 2018. Available from: https://digitalrepository.unm.edu/biol_etds/277

University of Illinois – Urbana-Champaign

12. Granger, Kyle L. A pilot study on the effects of sow management practices on piglet immune responsiveness to weaning stress.

Degree: MS, Animal Sciences, 2016, University of Illinois – Urbana-Champaign

URL: http://hdl.handle.net/2142/95266

► The consequences of maternal prenatal stress exposure of the gestating sow on the developing immune system of her offspring is not well understood. There is… (more)

▼ The consequences of maternal prenatal stress exposure of the gestating sow on the developing immune system of her offspring is not well understood. There is limited data that primarily focuses on the health and well-being of the neonates of livestock animals, principally within the swine industry, in relation to the presence of unavoidable production stressors, including—but not limited to—weaning, mixing and social hierarchy. Each of the aforementioned stressors has been previously shown to affect the health, well-being, performance and productivity of sows as well as exacerbate the disease process by compromising the immune system. Thus, more information is needed to elucidate the complex relationship between prenatal stressors and postnatal immunological competence of the offspring. The objective of this thesis was to assess the effects of sow housing environment, social stress, and dietary fiber treatments during gestation on the immune and stress responsiveness of their progeny to weaning stress. Piglets were obtained from a larger-scale study of a 180 group-housed gestating sows. Briefly, sows were randomly allotted to 1 of 2 high fiber gestation diets (1) 30% wheat middlings and 15% soybean hulls (MID-SOY) or 30% distillers dried grains and 30% corn germ meal (DDG-GM) and to a group pen with feeding stalls of either 0.6 m (SHT) or 1.8 m (LNG) in length. Sows were fed dietary treatments starting on gestational d 35 and then moved to treatment pens at gestational d 37 and kept until d 104. On d 37, prior to moving into their experimental pens, a subsample of sows were subjected to a dominance test by which we determined a dominance value (DV). Those sows with a high DV were labeled dominant (DOM) and those with a low DV were labeled submissive (SUB). From both the larger study and the subsample of sows, 40-42 piglets were selected (balanced across treatments) based on body weight prior to weaning, with the two heaviest and two lightest piglets from each litter being used. All piglets were weaned at 19 ± 2 d-of-age. Blood samples were taken 24h prior to weaning, and then 7 and 14 days post-weaning to assess descriptive and functional aspects of both innate and adaptive immunity and cortisol. These data revealed that piglets weaned from sows fed MID-SOY during gestation had a profile indicative of a skewed TH1 (cell-mediated) response, while piglets weaned from sows fed DDG-GM diet were skewed toward TH2 (humoral) response. Piglets from sows housed in pens with LNG feeding stalls were better able to cope with weaning stress compared to those piglets from sows housed in pens with SHT. Moreover, sow social status differentially impact piglet immune responsiveness to weaning stress. Piglets weaned from SUB sows had a greater cell-mediated immune response which may have cost them in terms of performance because piglets from DOM sows had improved performance. These results show that: (1) feeding gestating sows high fiber diets can impact the development and growth of her offspring; (2) physical environment of gestating… Advisors/Committee Members: Salak-Johnson, Janeen L (advisor), Gaskins, Rex (committee member), Dailey, Megan J (committee member).

Subjects/Keywords: adaptive immunity; gestation; innate immunity; piglet; weaning

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APA (6^th Edition):

Granger, K. L. (2016). A pilot study on the effects of sow management practices on piglet immune responsiveness to weaning stress. (Thesis). University of Illinois – Urbana-Champaign. Retrieved from http://hdl.handle.net/2142/95266

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):

Granger, Kyle L. “A pilot study on the effects of sow management practices on piglet immune responsiveness to weaning stress.” 2016. Thesis, University of Illinois – Urbana-Champaign. Accessed February 25, 2020. http://hdl.handle.net/2142/95266.

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

MLA Handbook (7^th Edition):

Granger, Kyle L. “A pilot study on the effects of sow management practices on piglet immune responsiveness to weaning stress.” 2016. Web. 25 Feb 2020.

Vancouver:

Granger KL. A pilot study on the effects of sow management practices on piglet immune responsiveness to weaning stress. [Internet] [Thesis]. University of Illinois – Urbana-Champaign; 2016. [cited 2020 Feb 25]. Available from: http://hdl.handle.net/2142/95266.

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

Council of Science Editors:

Granger KL. A pilot study on the effects of sow management practices on piglet immune responsiveness to weaning stress. [Thesis]. University of Illinois – Urbana-Champaign; 2016. Available from: http://hdl.handle.net/2142/95266

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

University of Alberta

13. Guntermann, Silvia. Caspase activity and regulation in Drosophila melanogaster innate immunity.

Degree: PhD, Department of Medical Microbiology and Immunology, 2014, University of Alberta

URL: https://era.library.ualberta.ca/files/cr207tp490

► The fine balance struck between life and death is key for the health of all multicellular organisms and therefore the pathways that govern life and… (more)

▼ The fine balance struck between life and death is key for the health of all multicellular organisms and therefore the pathways that govern life and death decisions are evolutionarily highly conserved. For example, the human TNF and the Drosophila IMD pathways coordinate signaling elements such as conserved JNK, NF-κB, and caspase modules to drive appropriate responses. Caspases are an evolutionarily conserved family of cysteinyl aspartate proteases with fundamental roles in the opposing processes of cell-survival and cell-death. The caspase Dredd is an essential pro-survival regulator of the IMD mediated immune response. However, the detailed involvement of Dredd in the sequential activation of the IMD cascade, the position of Dredd, and Dredd’s interactions with the IMD pathway were unknown. In addition, the molecular mechanism of Dredd activation and regulation was unclear. In this study I conducted a thorough structural and functional analysis of the mechanism of Dredd activity in IMD signaling. I revealed numerous interactions of Dredd with early activators of the IMD pathway. I showed that the caspase activity inhibitor p35 blocked Dredd activation in a mechanism that is distinct from the general mechanism of p35- dependent caspase inhibition. In addition, Dredd activation appears independent of auto-processing which might be explained by the lack of Dredd linker residues that support auto-processing and may explain Dredd’s sole function in pro- survival responses. In a combination of cell culture and in vivo assays, I demonstrated that Dredd is required for the activation of dJNK signaling upstream of dTAK1 and determined that Dredd additionally functions down- stream of Imd activation. Furthermore, my data uncovered a dual regulation of dIAP2 by RING domain mediated destruction and Dronc mediated N-terminal proteolytic cleavage. In summary, the data indicate a distinct activation mechanism for Dredd and establish dual functions for Dredd in the IMD signaling cascade, where Dredd is required in a proximal signaling complex for the early transduction of a phospho-relay to Rel and dJNK as well as for the subsequent activation of Rel. The data also uncover a novel role for Dronc in immune signaling. Combined the findings underline the importance and complexity of non-apoptotic roles of caspases.

Subjects/Keywords: innate immunity; caspase

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

APA (6^th Edition):

Guntermann, S. (2014). Caspase activity and regulation in Drosophila melanogaster innate immunity. (Doctoral Dissertation). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/cr207tp490

Chicago Manual of Style (16^th Edition):

Guntermann, Silvia. “Caspase activity and regulation in Drosophila melanogaster innate immunity.” 2014. Doctoral Dissertation, University of Alberta. Accessed February 25, 2020. https://era.library.ualberta.ca/files/cr207tp490.

MLA Handbook (7^th Edition):

Guntermann, Silvia. “Caspase activity and regulation in Drosophila melanogaster innate immunity.” 2014. Web. 25 Feb 2020.

Vancouver:

Guntermann S. Caspase activity and regulation in Drosophila melanogaster innate immunity. [Internet] [Doctoral dissertation]. University of Alberta; 2014. [cited 2020 Feb 25]. Available from: https://era.library.ualberta.ca/files/cr207tp490.

Council of Science Editors:

Guntermann S. Caspase activity and regulation in Drosophila melanogaster innate immunity. [Doctoral Dissertation]. University of Alberta; 2014. Available from: https://era.library.ualberta.ca/files/cr207tp490

Universiteit Utrecht

14. Fermie, J. Failure of Immunity Against Hepatitis C Virus: Implications of Defects in Early Immunity.

Degree: 2013, Universiteit Utrecht

URL: http://dspace.library.uu.nl:8080/handle/1874/283340

► The hepatitis C virus (HCV) is an upcoming human pathogen. Although HCV infection is mostly asymptomatic, persistent infection may lead to liver failure or liver… (more)

Subjects/Keywords: HCV; Hepatitis C Virus; Adaptive immunity; Innate immunity; T cell; chronic infection; viral immunity; immunity

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APA (6^th Edition):

Fermie, J. (2013). Failure of Immunity Against Hepatitis C Virus: Implications of Defects in Early Immunity. (Masters Thesis). Universiteit Utrecht. Retrieved from http://dspace.library.uu.nl:8080/handle/1874/283340

Chicago Manual of Style (16^th Edition):

Fermie, J. “Failure of Immunity Against Hepatitis C Virus: Implications of Defects in Early Immunity.” 2013. Masters Thesis, Universiteit Utrecht. Accessed February 25, 2020. http://dspace.library.uu.nl:8080/handle/1874/283340.

MLA Handbook (7^th Edition):

Fermie, J. “Failure of Immunity Against Hepatitis C Virus: Implications of Defects in Early Immunity.” 2013. Web. 25 Feb 2020.

Vancouver:

Fermie J. Failure of Immunity Against Hepatitis C Virus: Implications of Defects in Early Immunity. [Internet] [Masters thesis]. Universiteit Utrecht; 2013. [cited 2020 Feb 25]. Available from: http://dspace.library.uu.nl:8080/handle/1874/283340.

Council of Science Editors:

Fermie J. Failure of Immunity Against Hepatitis C Virus: Implications of Defects in Early Immunity. [Masters Thesis]. Universiteit Utrecht; 2013. Available from: http://dspace.library.uu.nl:8080/handle/1874/283340

University of Cambridge

15. Kaewert, Sarah. Immune-driven positive and balancing selection in human populations.

Degree: PhD, 2019, University of Cambridge

URL: https://www.repository.cam.ac.uk/handle/1810/293003

► This thesis examines the evidence for positive and balancing selection on immune genes in 388 individuals grouped into thirteen geographically diverse populations. The data are… (more)

▼ This thesis examines the evidence for positive and balancing selection on immune genes in 388 individuals grouped into thirteen geographically diverse populations. The data are high coverage whole genome sequences, many from populations that have been sparsely represented in global genetic diversity studies in the past. Two main analyses were performed for both positive and balancing selection: enrichment tests for each population and class of immune genes, and filtering for top variants or genes driving selection signals. Four different measures of positive selection and three measures of balancing selection were used to scan the whole genome data for evidence of selection. Further filters, including functional importance predictors, were used to filter results for potential driver variants. Positive selection results show significant enrichment for genes associated with bacteria or virus interaction, the innate immune system, and antigen processing and presentation. Results also include variants potentially driving signals of selection. One of these is a missense variant in the Northeast Siberian population in the gene IL27, which is involved in modulation of immune response to infection. Balancing selection enrichment tests show that genes associated with T cell function and antigen processing and presentation are significantly enriched in every population. The HLA region features heavily in these enrichments. One top gene result is GNLY, a gene that produces the antimicrobial protein granulysin, in the West Siberian and Island Southeast Asian populations. Another is PGLYRP4, which is a top gene in seven populations and is involved in recognition and defense against Gram-negative and -positive bacteria. In conclusion, as a general trend there is more enrichment in genes that interact with bacteria and viruses in the positive selection results, and more enrichment in genes involved with antigen processing and presentation and T cell function in the balancing selection results. The combined results show the different immune-driven selection histories of each population, as well as highlight a number of variants and genes that are potential drivers of selection and promising candidates for further study.

Subjects/Keywords: selection; immunity; genetics

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APA (6^th Edition):

Kaewert, S. (2019). Immune-driven positive and balancing selection in human populations. (Doctoral Dissertation). University of Cambridge. Retrieved from https://www.repository.cam.ac.uk/handle/1810/293003

Chicago Manual of Style (16^th Edition):

Kaewert, Sarah. “Immune-driven positive and balancing selection in human populations.” 2019. Doctoral Dissertation, University of Cambridge. Accessed February 25, 2020. https://www.repository.cam.ac.uk/handle/1810/293003.

MLA Handbook (7^th Edition):

Kaewert, Sarah. “Immune-driven positive and balancing selection in human populations.” 2019. Web. 25 Feb 2020.

Vancouver:

Kaewert S. Immune-driven positive and balancing selection in human populations. [Internet] [Doctoral dissertation]. University of Cambridge; 2019. [cited 2020 Feb 25]. Available from: https://www.repository.cam.ac.uk/handle/1810/293003.

Council of Science Editors:

Kaewert S. Immune-driven positive and balancing selection in human populations. [Doctoral Dissertation]. University of Cambridge; 2019. Available from: https://www.repository.cam.ac.uk/handle/1810/293003

Cornell University

16. Mouchka, Morgan. Microbial Friends And Foes: Characterizing The Cnidarian Response To Pathogenic And Mutualistic Microorganisms .

Degree: 2014, Cornell University

URL: http://hdl.handle.net/1813/36127

► The ecology and evolution of cnidarians is driven by symbiotic and pathogenic hostmicrobe relationships. Research regarding these relationships is especially timely given the recent decline… (more)

▼ The ecology and evolution of cnidarians is driven by symbiotic and pathogenic hostmicrobe relationships. Research regarding these relationships is especially timely given the recent decline of coral reef ecosystems, in part due to disruptions in cnidarian-microbe interactions. My dissertation is an experimental analysis of how cnidarians respond to both harmful and beneficial microorganisms and explores the interplay between these two types of interactions. Corals provide a multifaceted habitat that supports a rich bacterial assemblage, and in Chapter 1, I review our current knowledge regarding the diversity, specificity, development, and functions of these assemblages. With a meta-analysis of previous work, I quantitatively analyze what is known regarding the relationship between coral-associated microorganisms and disease. Finally, I examine evidence that these populations could be disrupted by climatic change. One of the most well-known mutualistic relationships is that between cnidarians and unicellular dinoflagellates. To evaluate the molecular mechanisms that underlie the persistence of this relationship, in Chapter 2, I identify differentially expressed transcripts between symbiotic and aposymbiotic individuals of the model sea anemone, Aiptasia pallida. These transcripts include those with potential functions in several metabolic pathways, transport of nutrients between the partners, and host tolerance of the dinoflagellate. To broaden our understanding of the cnidarian response to pathogenic microbes, in Chapter 3, I report the host transcriptome response of aposymbiotic Aiptasia to experimental inoculation with Serratia marcescens. My results suggest that Aiptasia responds to bacterial challenge via the regulation of tumor necrosis factor receptor-associated factor-mediated signaling, apoptosis, and ubiquitination, thus suggesting that lower metazoans respond to immune challenge via highly conserved mechanisms. To determine how the Aiptasia immune response is modulated via the presence of dinoflagellate symbionts, in Chapter 4, I compared gene expression and behavioral assays of S. marcescens-exposed anemones with and without their symbionts. The presence of dinoflagellates greatly alters the number and type of genes expressed in response to bacterial challenge. In addition, symbiotic anemones were less likely to recover from pathogen exposure and had lower survival rates than their aposymbiotic counterparts. These results are consistent with the hypothesis that symbiotic dinoflagellates suppress Aiptasia immunity, perhaps to promote symbiotic homeostasis. Advisors/Committee Members: Lazzaro, Brian (committeeMember), Searle, Angela E. (committeeMember), (committeeMember).

Subjects/Keywords: cnidarian; immunity; microorganisms

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APA (6^th Edition):

Mouchka, M. (2014). Microbial Friends And Foes: Characterizing The Cnidarian Response To Pathogenic And Mutualistic Microorganisms . (Thesis). Cornell University. Retrieved from http://hdl.handle.net/1813/36127

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):

Mouchka, Morgan. “Microbial Friends And Foes: Characterizing The Cnidarian Response To Pathogenic And Mutualistic Microorganisms .” 2014. Thesis, Cornell University. Accessed February 25, 2020. http://hdl.handle.net/1813/36127.

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

MLA Handbook (7^th Edition):

Mouchka, Morgan. “Microbial Friends And Foes: Characterizing The Cnidarian Response To Pathogenic And Mutualistic Microorganisms .” 2014. Web. 25 Feb 2020.

Vancouver:

Mouchka M. Microbial Friends And Foes: Characterizing The Cnidarian Response To Pathogenic And Mutualistic Microorganisms . [Internet] [Thesis]. Cornell University; 2014. [cited 2020 Feb 25]. Available from: http://hdl.handle.net/1813/36127.

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

Council of Science Editors:

Mouchka M. Microbial Friends And Foes: Characterizing The Cnidarian Response To Pathogenic And Mutualistic Microorganisms . [Thesis]. Cornell University; 2014. Available from: http://hdl.handle.net/1813/36127

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

Rutgers University

17. Pierre, Kamau, 1987-. Evaluation of the role of cortisol in modulating seasonal changes in immunity.

Degree: PhD, Biomedical Engineering, 2017, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/55618/

►

Inflammatory diseases such as asthma, rheumatoid arthritis (RA) and systemic vasculitis exhibit seasonality with higher prevalence and aggravated symptoms occurring during the winter months. Though… (more)

▼

Inflammatory diseases such as asthma, rheumatoid arthritis (RA) and systemic vasculitis exhibit seasonality with higher prevalence and aggravated symptoms occurring during the winter months. Though the underlying causes remain to be elucidated, disease seasonality has been associated with circannual changes in antibodies, hormonal levels, acute phase reactants and numerous immunomodulatory components. For instance, RA risk biomarkers such as IL-6R mRNA, sIL-6 receptor and C-reactive proteins vary significantly throughout the year with peak expressions during the winter season. Apart from seasonal variation, the dynamics of functions such as cytokine production and hormone secretion display diurnal fluctuations that are entrained to the external 24-hour light/dark cycle. The light fraction of the light/dark cycle, or photoperiod, varies predictably throughout the year and is a robust environmental cue that synchronizes seasonal variations in neuroendocrine function. It is well established that cortisol, regulated via hypothalamic-pituitary-adrenal (HPA) axis activity and entrained to the external photoperiod, is a potent immunomodulator whose level varies seasonally. A detailed experimental analysis of the role of the HPA axis in regulating seasonal changes in immune function is lacking due to the complex network of biological interactions. In this work, we developed a semi-mechanistic mathematical model to evaluate cortisol’s role in modulating seasonal immunological plasticity. Our results indicate a shift from an anti- to a pro-inflammatory state as the seasons progress from summer through winter with elevated expression of the cortisol-activating enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1), an inflammatory disease biomarker, predicted for the winter season. Experimentally, the pro-inflammatory phenotype correlated with mitotic asynchrony is mitigated following glucocorticoid-induced cell resynchronization. A cortisol-dependent, time-of-day and seasonal variability in the synchronization of the molecular clock and cell cycle was predicted. These findings have major health implications as the misalignment of internal dynamics with environmental signals has been associated with inflammatory disease progression. The current model provides a framework for exploring the impact of asynchrony between the circadian and cell cycle oscillators, amongst cells in a population, on immune system dynamics. Knowledge of the underlying putative mechanisms governing seasonal and diurnal modifications of immune system dynamics can be applied to design more effective preventative and chronotherapeutic strategies addressing the development and advancement of a pro-inflammatory state.

Advisors/Committee Members: Androulakis, Ioannis P (chair), Hacihaliloglu, Ilker (internal member), Shinbrot, Troy (internal member), Schlesinger, Naomi (outside member), School of Graduate Studies.

Subjects/Keywords: Cortisol; Immunity system

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APA (6^th Edition):

Pierre, Kamau, 1. (2017). Evaluation of the role of cortisol in modulating seasonal changes in immunity. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/55618/

Chicago Manual of Style (16^th Edition):

Pierre, Kamau, 1987-. “Evaluation of the role of cortisol in modulating seasonal changes in immunity.” 2017. Doctoral Dissertation, Rutgers University. Accessed February 25, 2020. https://rucore.libraries.rutgers.edu/rutgers-lib/55618/.

MLA Handbook (7^th Edition):

Pierre, Kamau, 1987-. “Evaluation of the role of cortisol in modulating seasonal changes in immunity.” 2017. Web. 25 Feb 2020.

Vancouver:

Pierre, Kamau 1. Evaluation of the role of cortisol in modulating seasonal changes in immunity. [Internet] [Doctoral dissertation]. Rutgers University; 2017. [cited 2020 Feb 25]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/55618/.

Council of Science Editors:

Pierre, Kamau 1. Evaluation of the role of cortisol in modulating seasonal changes in immunity. [Doctoral Dissertation]. Rutgers University; 2017. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/55618/

18. Evans, John W., III. Itk is a Dual Action Regulator of Immunoreceptor Signaling in the Innate and Adaptive Immune System: A Dissertation.

Degree: Immunology and Microbiology, Pathology, 2013, U of Massachusetts : Med

URL: http://escholarship.umassmed.edu/gsbs_diss/688

► The cells and molecules that comprise the immune system are essential for mounting an effective response against microbes. A successful immune response limits pathology… (more)

▼ The cells and molecules that comprise the immune system are essential for mounting an effective response against microbes. A successful immune response limits pathology within the host while simultaneously eliminating the pathogen. The key to this delicate balance is the correct recognition of the pathogen and the appropriate response of immune cells. Cellular activation originates through receptors that relay information about the state of the microenvironment to different compartments within the cell. The rapid relay of information is called signal transduction and employs a network of signaling mediators such as kinases, phosphatases, adaptor molecules, and transcription factors. IL-2 inducible T cell kinase (Itk) is a non-receptor tyrosine kinase that is an integral component of signal transduction downstream of many immunoreceptors. This dissertation describes two distinct pathways that utilize Itk in both phases of the immune response. T cells use the TCR to sense a multitude of peptide-based ligands and to transmit signals inside the cell to activate cellular function. In this regard, the diversity of ligands the T cells encounter can be portrayed as analog inputs. Once a critical threshold is met, signaling events transpire in close proximity to the plasma membrane to activate major downstream pathways in the cell. The majority of these pathways are digital in nature resulting in the on or off activation of T cells. We find, however, that altering the TCR signal strength that a T cell receives can result in an analog-based response. Here, the graded expression of a transcription factor, IRF4, is modulated through the activity of Itk. We link this graded response to an NFAT-mediated pathway in which the digital vs. analog nature has been previously uncharacterized. Finally, we demonstrate that the repercussions of an analog signaling pathway is the altered expression of a second transcription factor, Eomes, which is important in the differentiation and function of T cells. These results suggest that Itk is crucial in the modulation of TCR signal strength. Mast cells primarily rely on the IgE-bound FcεR1 for pathogen recognition. Crosslinking this receptor activates mast cells and results in degranulation and cytokine production via an expansive signaling cascade. Upon stimulation, Itk is recruited to the plasma membrane and phosphorylated. Little else is known about how Itk operates inside of mast cells. We find that mast cells lacking Itk are hyperresponsive to FcεR1-mediated activation. This is most apparent in the amount of IL-4 and IL-13 produced in comparison to wild-type mast cells. Increased cytokine production was accompanied by elevated and sustained signaling downstream of the FcεR1. Finally, biochemical evidence demonstrates that Itk is part of an inhibitory complex containing the phosphatase SHIP-1. These results indicate a novel function for Itk as a negative regulator in FcεR1- mediated mast cell activation. Advisors/Committee Members: Leslie J. Berg, PhD.

Subjects/Keywords: Signal Transduction; Protein-Tyrosine Kinases; Adaptive Immunity; Innate Immunity; Immunity; Immunopathology

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APA (6^th Edition):

Evans, John W., I. (2013). Itk is a Dual Action Regulator of Immunoreceptor Signaling in the Innate and Adaptive Immune System: A Dissertation. (Doctoral Dissertation). U of Massachusetts : Med. Retrieved from http://escholarship.umassmed.edu/gsbs_diss/688

Chicago Manual of Style (16^th Edition):

Evans, John W., III. “Itk is a Dual Action Regulator of Immunoreceptor Signaling in the Innate and Adaptive Immune System: A Dissertation.” 2013. Doctoral Dissertation, U of Massachusetts : Med. Accessed February 25, 2020. http://escholarship.umassmed.edu/gsbs_diss/688.

MLA Handbook (7^th Edition):

Evans, John W., III. “Itk is a Dual Action Regulator of Immunoreceptor Signaling in the Innate and Adaptive Immune System: A Dissertation.” 2013. Web. 25 Feb 2020.

Vancouver:

Evans, John W. I. Itk is a Dual Action Regulator of Immunoreceptor Signaling in the Innate and Adaptive Immune System: A Dissertation. [Internet] [Doctoral dissertation]. U of Massachusetts : Med; 2013. [cited 2020 Feb 25]. Available from: http://escholarship.umassmed.edu/gsbs_diss/688.

Council of Science Editors:

Evans, John W. I. Itk is a Dual Action Regulator of Immunoreceptor Signaling in the Innate and Adaptive Immune System: A Dissertation. [Doctoral Dissertation]. U of Massachusetts : Med; 2013. Available from: http://escholarship.umassmed.edu/gsbs_diss/688

19. Schrum, Jacob E. Pathways Involved in Recognition and Induction of Trained Innate Immunity by Plasmodium falciparum.

Degree: PhD, Department of Medicine, Division of Infectious Diseases and Immunology, 2017, U of Massachusetts : Med

URL: http://escholarship.umassmed.edu/gsbs_diss/917

► Malarial infection in naïve individuals induces a robust innate immune response, but our understanding of the mechanisms by which the innate immune system recognizes… (more)

Subjects/Keywords: Plasmodium falciparum; innate immunity; innate immune memory; cGAS; trained immunity; Immunity; Immunology of Infectious Disease

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APA (6^th Edition):

Schrum, J. E. (2017). Pathways Involved in Recognition and Induction of Trained Innate Immunity by Plasmodium falciparum. (Doctoral Dissertation). U of Massachusetts : Med. Retrieved from http://escholarship.umassmed.edu/gsbs_diss/917

Chicago Manual of Style (16^th Edition):

Schrum, Jacob E. “Pathways Involved in Recognition and Induction of Trained Innate Immunity by Plasmodium falciparum.” 2017. Doctoral Dissertation, U of Massachusetts : Med. Accessed February 25, 2020. http://escholarship.umassmed.edu/gsbs_diss/917.

MLA Handbook (7^th Edition):

Schrum, Jacob E. “Pathways Involved in Recognition and Induction of Trained Innate Immunity by Plasmodium falciparum.” 2017. Web. 25 Feb 2020.

Vancouver:

Schrum JE. Pathways Involved in Recognition and Induction of Trained Innate Immunity by Plasmodium falciparum. [Internet] [Doctoral dissertation]. U of Massachusetts : Med; 2017. [cited 2020 Feb 25]. Available from: http://escholarship.umassmed.edu/gsbs_diss/917.

Council of Science Editors:

Schrum JE. Pathways Involved in Recognition and Induction of Trained Innate Immunity by Plasmodium falciparum. [Doctoral Dissertation]. U of Massachusetts : Med; 2017. Available from: http://escholarship.umassmed.edu/gsbs_diss/917

University of Utah

20. Bareyan, Diana H. Studies of vaccine adjuvants that can elicit the generation of mucosal immune responses to cutaneously delivered antigens;.

Degree: MS;, Pathology;, 2007, University of Utah

URL: http://content.lib.utah.edu/cdm/singleitem/collection/etd1/id/410/rec/1263

► Vaccines are designed to protect against infectious diseases. The majority of commercially available vaccines are administered to hosts via parenteral routes and provoke the development… (more)

▼ Vaccines are designed to protect against infectious diseases. The majority of commercially available vaccines are administered to hosts via parenteral routes and provoke the development of only systemic immunity. However, most pathogens infect susceptible hosts by crossing a mucosal barrier. The development of vaccines capable of eliciting both systemic and mucosal immune responses would be desirable, and provide better protection to immunized hosts. Our laboratory previously reported that the bioactive form of vitamin D3, la25(OH)2D3, when added to vaccines and administered cutaneously, induces both systemic and mucosal immune responses. It was established that antigen-laden dendritic cells (DCs) can bypass draining lymph node (LN) sequestration and localize to classical inductive sites of mucosal immunity when exposed to la25(OH)2D3 during their maturation. In Chapter 2 of this thesis, we demonstrate that la25(OH)2D3-exposed skin residing DCs can bypass the draining LN and localize to various non-draining LNs and Peyer's patches (PPs). The responsible mechanism involves a temporal suppression in the activation-induced upregulation of CCR7, resulting in a depressed chemotaxis toward CCL21 (a ligand for CCR7). The suppression is transient and normal chemotactic activities are required over time. Pathogen recognition is achieved in part through Toll-like receptors (TLRs) that are members of the pattern-recognition receptor family. Innate immune responses that are initiated by TLR activation can influence subsequent events and regulate the types of adaptive immune responses that develop. In Chapter 3 of this thesis, natural ligands for TLR3, TLR4 and TLR9 were examined for possible roles as adjuvants in the generation of systemic and mucosal immune responses. DCs activated with TLR3 or TLR4 ligands were able to upregulate the expression of 25-hydroxycholecalciferol-la-hydroxylase, an enzyme that catalyzes the conversion of bioinactive 25-hydroxyvitamin D3 to the active la25(OH)2D3. Also, TLR3/4-activated DCs exhibited altered migratory properties in vivo through a la25(OH)2D3 -dependent processes. Our results suggest that the successful generation of mucosal immunity to antigens administered cutaneously, might best be achieved when endogenously produced, or exogenously administered lot25(OH)2D3, is available.

Subjects/Keywords: Myeloid Dendritic Cell; Muscosal Immunity

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APA (6^th Edition):

Bareyan, D. H. (2007). Studies of vaccine adjuvants that can elicit the generation of mucosal immune responses to cutaneously delivered antigens;. (Masters Thesis). University of Utah. Retrieved from http://content.lib.utah.edu/cdm/singleitem/collection/etd1/id/410/rec/1263

Chicago Manual of Style (16^th Edition):

Bareyan, Diana H. “Studies of vaccine adjuvants that can elicit the generation of mucosal immune responses to cutaneously delivered antigens;.” 2007. Masters Thesis, University of Utah. Accessed February 25, 2020. http://content.lib.utah.edu/cdm/singleitem/collection/etd1/id/410/rec/1263.

MLA Handbook (7^th Edition):

Bareyan, Diana H. “Studies of vaccine adjuvants that can elicit the generation of mucosal immune responses to cutaneously delivered antigens;.” 2007. Web. 25 Feb 2020.

Vancouver:

Bareyan DH. Studies of vaccine adjuvants that can elicit the generation of mucosal immune responses to cutaneously delivered antigens;. [Internet] [Masters thesis]. University of Utah; 2007. [cited 2020 Feb 25]. Available from: http://content.lib.utah.edu/cdm/singleitem/collection/etd1/id/410/rec/1263.

Council of Science Editors:

Bareyan DH. Studies of vaccine adjuvants that can elicit the generation of mucosal immune responses to cutaneously delivered antigens;. [Masters Thesis]. University of Utah; 2007. Available from: http://content.lib.utah.edu/cdm/singleitem/collection/etd1/id/410/rec/1263

University of Utah

21. Zhang, Tian Yi. Programming of immune responsiveness by end-organ metabolism of glucocorticoids.

Degree: PhD, Pathology;, 2007, University of Utah

URL: http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/20/rec/936

► 11beta-Hydroxysteroid Dehydrogenase Type 1 (11betaHSD1) catalyzes the conversion of C11-keto-glucocorticoids (GCs) to bioactive C11-hydroxy-GCs, thereby generating activating ligands for the glucocorticoid receptor. We demonstrate that… (more)

▼ 11beta-Hydroxysteroid Dehydrogenase Type 1 (11betaHSD1) catalyzes the conversion of C11-keto-glucocorticoids (GCs) to bioactive C11-hydroxy-GCs, thereby generating activating ligands for the glucocorticoid receptor. We demonstrate that immune cells of both lymphoid (immature thymocytes, CD4+/CD8+ T cells and B220+ B cells) and myeloid (CD11b+ macrophages (M-phi-s). CD11c+ dendrite cells) lineages possess 11betaHSD1 reductase activity. Activation of wild-type, but not 11betaHSD1-/- CD4+ T cells in the presence of C11-keto-GCs attenuates IFN-gamma and IL-2 production. The ability of 11betaHSD1+/+ CD4+ T cells to generate bioactive GCs via intracellular 11betaHSD1 allows a degree of autonomous control over lymphocyte biology and effector functions. Mice deficient in 11betaHSD1 exhibit a proinflammatory phenotype in vivo, as evidenced by the accelerated weight loss and elevated serum TNFalpha, IL-12p40 levels following LPS challenge. 11betaHSD1-/- splenic M-phi-s (splnM-phi-s) and B cells contribute to the inflammatory phenotype since they over express inflammatory cytokines following LPS stimulation. 11betaHSD1+/+ and 11betaHSD1-/- bone marrow derived M-phi-s (BMM-phi-s) acquire and inflammatory phenotype only following conditioning with low levels of GCs, suggesting the hyperresponsiveness of 11betaHSD1-/- splinM-phi-s does not result from intrinsic 11betaHSD1 deficiency. Instead, the proinflammatory phenotype of 11betaHSD1-/- splnM-phi-s results from differential differentiation within the 11betaHSD1-/- host microenvironment, when plasma GC levels are moderately elevated. The overproduction of inflammatory cytokines by GC-conditioned BMM-phi-s and 11betaHSD1-/- splnM-phi-s appears to result from increased activation of the NFkB and MAP kinase signaling cascades, and an attenuation of P13K-dependent Akt activation. Additionally, 11betaHSD1-/- splnM-phi-s and GC conditioned BMM-phi-s express significantly more Src-homology 2 containing 5’ phosphatase 1 (SHIP1), which appears to be responsible for the depression in Akt activation. The presence of neutralizing antibodies for TGFbeta abrogates the ability of GCs to enhance SHIP1 expression in BMM-phi-s, suggesting GCs upregulate SHIP1 expression via induction to TGF-beta expression. Consistently, cultures of GC-conditioned BMM-phi-s and CD11b- immune cells obtained from the BM and spleen 11betaHSD1-/- mice express increased levels of bioactive TGFbeta. Our results suggest that modest elevations in micro-environmental GC levels can modify M-phi differentiation and thereby influence subsequent responses to stimulation.

Subjects/Keywords: immunity; Metabolism; Immue Response

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APA (6^th Edition):

Zhang, T. Y. (2007). Programming of immune responsiveness by end-organ metabolism of glucocorticoids. (Doctoral Dissertation). University of Utah. Retrieved from http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/20/rec/936

Chicago Manual of Style (16^th Edition):

Zhang, Tian Yi. “Programming of immune responsiveness by end-organ metabolism of glucocorticoids.” 2007. Doctoral Dissertation, University of Utah. Accessed February 25, 2020. http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/20/rec/936.

MLA Handbook (7^th Edition):

Zhang, Tian Yi. “Programming of immune responsiveness by end-organ metabolism of glucocorticoids.” 2007. Web. 25 Feb 2020.

Vancouver:

Zhang TY. Programming of immune responsiveness by end-organ metabolism of glucocorticoids. [Internet] [Doctoral dissertation]. University of Utah; 2007. [cited 2020 Feb 25]. Available from: http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/20/rec/936.

Council of Science Editors:

Zhang TY. Programming of immune responsiveness by end-organ metabolism of glucocorticoids. [Doctoral Dissertation]. University of Utah; 2007. Available from: http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/20/rec/936

Universiteit Utrecht

22. Kamp, M.E. Immunity to schistosomes in man and snail.

Degree: 2014, Universiteit Utrecht

URL: http://dspace.library.uu.nl:8080/handle/1874/301207

► Schistosomiasis is a parasitic disease found in tropical areas, caused by fluke worms of the genus Schistosoma (S.). This parasite can infect humans and other… (more)

Subjects/Keywords: Schistosomiasis; immunity; resistance; FREP

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APA (6^th Edition):

Kamp, M. E. (2014). Immunity to schistosomes in man and snail. (Masters Thesis). Universiteit Utrecht. Retrieved from http://dspace.library.uu.nl:8080/handle/1874/301207

Chicago Manual of Style (16^th Edition):

Kamp, M E. “Immunity to schistosomes in man and snail.” 2014. Masters Thesis, Universiteit Utrecht. Accessed February 25, 2020. http://dspace.library.uu.nl:8080/handle/1874/301207.

MLA Handbook (7^th Edition):

Kamp, M E. “Immunity to schistosomes in man and snail.” 2014. Web. 25 Feb 2020.

Vancouver:

Kamp ME. Immunity to schistosomes in man and snail. [Internet] [Masters thesis]. Universiteit Utrecht; 2014. [cited 2020 Feb 25]. Available from: http://dspace.library.uu.nl:8080/handle/1874/301207.

Council of Science Editors:

Kamp ME. Immunity to schistosomes in man and snail. [Masters Thesis]. Universiteit Utrecht; 2014. Available from: http://dspace.library.uu.nl:8080/handle/1874/301207

University of Utah

23. Trunnell, Eric Phillip. Investigation into the protective processes involved when C3Hf/St inbred mice are infected with Hymenolepis Citelli;.

Degree: MS;, Biomedical Informatics;, 1977, University of Utah

URL: http://content.lib.utah.edu/cdm/singleitem/collection/etd1/id/1680/rec/714

► A model system was established in investigate host-parasite relationships using C3Hf/St inbred mice as the host, and Hymenolepis citelli McLeod as the non-invasive intestinal dwelling… (more)

▼ A model system was established in investigate host-parasite relationships using C3Hf/St inbred mice as the host, and Hymenolepis citelli McLeod as the non-invasive intestinal dwelling cestode. The C3H mice proved to be highly susceptible to infections of H. citelli, in that about 50% of the cysticercoids administered developed into adult worms. Primary infections of ten cysticercoids per mouse appeared to result in a low grade protective response beginning 21 days post infection. In addition, a form of protective response appeared with secondary infections of ten cysticercoids, when preceded by an initial infection of ten cysticercoids followed by a booster of five cysticercoids. This protection may be influenced by physiological factors; such as crowding and competition, and/or the use of an antihelmintic that could increase the potential infect ability by depressing the host responses. This model provides a system that allows more controlled experiments and is the initial step in investigations leading to a definitive understanding of the protective mechanisms responsible for the host’s response to the parasite. Specific antibody has been demonstrated in the serum and directly on the worm taken from C3H mice infected with H. citelli by using immunofluorescence. Anti-H citelli antibodies of both IgG and IgA classes were found within the serum, and directly on sections of worms taken from infected mice. Stronger IgG specific fluorescence was observed in the serum, while IgA was the predominant class of antibody found on sections of worm taken directly for the gut of infected mice. A kinetic analysis of the humoral and secretory components following a primary infection of ten cysticercoids revealed the ability to detect antibody in the serum as well as directly on sections approximately three weeks post infection. Interestingly, antibody was only detectable on worms taken between three and five weeks post infection. No antibody was detectable on worms taken from mice with greater than five week only infections. It was, however, possible to detect the presence of antibody in concentrated intestinal chyme and fecal pellets taken from mice previously infected for 35 to 39 days. The relationship between these observations and the natural history of H. citelli infections in C3H mice are discussed.

Subjects/Keywords: Immunity; Infectioins

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APA (6^th Edition):

Trunnell, E. P. (1977). Investigation into the protective processes involved when C3Hf/St inbred mice are infected with Hymenolepis Citelli;. (Masters Thesis). University of Utah. Retrieved from http://content.lib.utah.edu/cdm/singleitem/collection/etd1/id/1680/rec/714

Chicago Manual of Style (16^th Edition):

Trunnell, Eric Phillip. “Investigation into the protective processes involved when C3Hf/St inbred mice are infected with Hymenolepis Citelli;.” 1977. Masters Thesis, University of Utah. Accessed February 25, 2020. http://content.lib.utah.edu/cdm/singleitem/collection/etd1/id/1680/rec/714.

MLA Handbook (7^th Edition):

Trunnell, Eric Phillip. “Investigation into the protective processes involved when C3Hf/St inbred mice are infected with Hymenolepis Citelli;.” 1977. Web. 25 Feb 2020.

Vancouver:

Trunnell EP. Investigation into the protective processes involved when C3Hf/St inbred mice are infected with Hymenolepis Citelli;. [Internet] [Masters thesis]. University of Utah; 1977. [cited 2020 Feb 25]. Available from: http://content.lib.utah.edu/cdm/singleitem/collection/etd1/id/1680/rec/714.

Council of Science Editors:

Trunnell EP. Investigation into the protective processes involved when C3Hf/St inbred mice are infected with Hymenolepis Citelli;. [Masters Thesis]. University of Utah; 1977. Available from: http://content.lib.utah.edu/cdm/singleitem/collection/etd1/id/1680/rec/714

Texas Medical Center

24. Rodriguez-Cruz, Tania G. THE CYTOPLASMIC TAIL OF MHC CLASS I MOLECULES PLAYS A CRITICAL ROLE IN DENDRITIC CELL-INDUCED T CELL IMMUNITY.

Degree: PhD, 2011, Texas Medical Center

URL: http://digitalcommons.library.tmc.edu/utgsbs_dissertations/243

► The presentation of MHC class I (MHC-I)/peptide complexes by dendritic cells (DCs) is critical for the maintenance of central tolerance to self and for… (more)

▼ The presentation of MHC class I (MHC-I)/peptide complexes by dendritic cells (DCs) is critical for the maintenance of central tolerance to self and for the regulation of cytotoxic T lymphocytes (CTL)-mediated adaptive immune responses against pathogens and cancer cells. Interestingly, several findings have suggested that the cytoplasmic tail of MHC class I plays a functional role in the regulation of CTL immune responses. For example, our previous studies demonstrated that exon 7-deleted MHC-I molecules not only showed extended DC cell surface half-lives but also induced significantly increased CTL responses to viral challange invivo. Although exon 7-deleted variant of MHC-I does not occur naturally in humans, the animal studies prompted us to examine whether exon 7-deleted MHC-I molecules could generate augmented CTL responses in a therapeutic DC-based vaccine setting. To examine the stimulatory capacity of exon 7-deleted MHC-I molecules, we generated a lentivirus-mediated gene transfer system to induce the expression of different MHC-I cytoplasmic tail isoforms in both mouse and human DCs. These DCs were then used as vaccines in a melanoma mouse tumor model and in a human invitro co-culture system. In this thesis, we show that DCs expressing exon 7-deleted MHC-I molecules, stimulated remarkably higher levels of T-cell cytokine production and significantly increased the proliferation of meanoma-specific (Pmel-1) T cells compared with DCs expressing wild type MHC-I. We also demonstrate that, in combination with adoptive transfer of Pmel-1 T-cell, DCs expressing exon 7-deleted Db molecules induced greater anti-tumor responses against established B16 melanoma tumors, significantly extending mouse survival as compared to DCs expressing wild-type Db molecules. Moreover, we also observed that human DCs expressing exon 7-deleted HLA-A2 molecules showed similarly augmented CTL stimulatory ability. Mechanistic studies suggest that exon 7-deleted MHC-I molecules showed impaired lateral membrane movement and extended cell surface half-lives within the DC/T-cell interface, leading to increased spatial availability of MHC-I/peptide complexes for recognition by CD8+ T cells. Collectively, these results suggesr that targeting exon 7 within the cytoplasmic tail of MHC-I molecules in DC vaccines has the potential to enhance CD8+ T cell stimulatory capacity and improve clinical outcomes in patients with cancer or viral infections. Advisors/Committee Members: Gregory Lizee, Patrick Hwu, Stephanie Watowich.

Subjects/Keywords: Immunity; Medicine and Health Sciences

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APA (6^th Edition):

Rodriguez-Cruz, T. G. (2011). THE CYTOPLASMIC TAIL OF MHC CLASS I MOLECULES PLAYS A CRITICAL ROLE IN DENDRITIC CELL-INDUCED T CELL IMMUNITY. (Doctoral Dissertation). Texas Medical Center. Retrieved from http://digitalcommons.library.tmc.edu/utgsbs_dissertations/243

Chicago Manual of Style (16^th Edition):

Rodriguez-Cruz, Tania G. “THE CYTOPLASMIC TAIL OF MHC CLASS I MOLECULES PLAYS A CRITICAL ROLE IN DENDRITIC CELL-INDUCED T CELL IMMUNITY.” 2011. Doctoral Dissertation, Texas Medical Center. Accessed February 25, 2020. http://digitalcommons.library.tmc.edu/utgsbs_dissertations/243.

MLA Handbook (7^th Edition):

Rodriguez-Cruz, Tania G. “THE CYTOPLASMIC TAIL OF MHC CLASS I MOLECULES PLAYS A CRITICAL ROLE IN DENDRITIC CELL-INDUCED T CELL IMMUNITY.” 2011. Web. 25 Feb 2020.

Vancouver:

Rodriguez-Cruz TG. THE CYTOPLASMIC TAIL OF MHC CLASS I MOLECULES PLAYS A CRITICAL ROLE IN DENDRITIC CELL-INDUCED T CELL IMMUNITY. [Internet] [Doctoral dissertation]. Texas Medical Center; 2011. [cited 2020 Feb 25]. Available from: http://digitalcommons.library.tmc.edu/utgsbs_dissertations/243.

Council of Science Editors:

Rodriguez-Cruz TG. THE CYTOPLASMIC TAIL OF MHC CLASS I MOLECULES PLAYS A CRITICAL ROLE IN DENDRITIC CELL-INDUCED T CELL IMMUNITY. [Doctoral Dissertation]. Texas Medical Center; 2011. Available from: http://digitalcommons.library.tmc.edu/utgsbs_dissertations/243

Texas A&M University

25. Jiang, Shan. Plant Defense Signaling Mechanisms and Evolution.

Degree: 2015, Texas A&M University

URL: http://hdl.handle.net/1969.1/155604

► Plant innate immunity has been classified into two layers of defense systems. Nucleotide-binding domain leucine-rich repeat (NLR) protein complexes activated by pathogen effectors launches effector-triggered… (more)

▼ Plant innate immunity has been classified into two layers of defense systems. Nucleotide-binding domain leucine-rich repeat (NLR) protein complexes activated by pathogen effectors launches effector-triggered immunity (ETI). A forward genetic screen using the ETI marker gene WRKY46 promoter fused with a firefly luciferase gene (pWRKY46::LUC) as a reporter identified five ARABIDOPSIS GENES GOVERNING IMMUNE GENE EXPRESSION (aggie) mutants, named as aggie4-8. Though with elevated pWRKY46::LUC activity, aggie4 showed enhanced resistance to avirulent bacterial infections, yet delayed hypersensitive response (HR), while aggie5 exhibited compromised disease resistance and delayed HR. Map-based cloning coupled with next generation sequencing (NGS) suggests that causal mutations of aggie4 and aggie5 locate in different regions of chromosome 5. In addition, pWRKY46::LUC activity is elevated in aggie6 and aggie7, while suppressed in aggie8. Perception of microbe-associated molecular patterns (MAMPs) by pattern recognition receptors (PRRs) triggers another tier of innate immunity, termed as pattern-triggered immunity (PTI). The Arabidopsis SOMATIC EMBRYOGENESIS RECEPTOR KINASE (SERK) family plays important roles in plant defense responses. It remains unknown how SERK members have evolved. Here, three SERK homologs, Pp1s35_219V6.1, Pp1s96_90V6.1 and Pp1s118_79V6.1 were identified in P. Patens with 60%-80% amino acid identify to AtSERKs and were named as PpSERK1.1, PpSERK1.2 and PpSERK2 respectively. In vitro kinase assay revealed that PpSERK1.1 and PpSERK1.2, but not PpSERK2, possess strong kinase activity. Functional complementation analysis suggested that PpSERK1.1 and PpSERK1.2 but not PpSERK2 regulate FLS2-mediated plant defense, and PpSERK1.2 but not PpSERK1.1 also regulates cell death in Arabidopsis. PTI induces a rapid and profound transcriptional reprograming via concerted actions of specific transcription factors and general transcription machinery. Arabidopsis SH4-related 3 (ASR3), a plant specific trihelix family of transcription factors, is rapidly phosphorylated by MPK4 at Threonine 189 residue upon multiple MAMP treatments but not upon elicitation of ETI. Genetic and biochemical data suggests that phosphorylation of ASR3 enhances its DNA binding activity to suppress immune genes expression. Importantly, the asr3 mutant shows higher immune gene activation and enhanced disease resistance, while transgenic plants overexpressing ASR3 exhibit compromised PTI responses. This study reveals that ASR3 functions as a transcription repressor regulated by MPK4 to fine-tune plant defense. Advisors/Committee Members: Shan, Libo (advisor), He, Ping (committee member), Kenerley, Charles (committee member), Figueiredo, Paul de (committee member).

Subjects/Keywords: Plant defense; innate immunity; evolution

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APA (6^th Edition):

Jiang, S. (2015). Plant Defense Signaling Mechanisms and Evolution. (Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/155604

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):

Jiang, Shan. “Plant Defense Signaling Mechanisms and Evolution.” 2015. Thesis, Texas A&M University. Accessed February 25, 2020. http://hdl.handle.net/1969.1/155604.

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

MLA Handbook (7^th Edition):

Jiang, Shan. “Plant Defense Signaling Mechanisms and Evolution.” 2015. Web. 25 Feb 2020.

Vancouver:

Jiang S. Plant Defense Signaling Mechanisms and Evolution. [Internet] [Thesis]. Texas A&M University; 2015. [cited 2020 Feb 25]. Available from: http://hdl.handle.net/1969.1/155604.

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

Council of Science Editors:

Jiang S. Plant Defense Signaling Mechanisms and Evolution. [Thesis]. Texas A&M University; 2015. Available from: http://hdl.handle.net/1969.1/155604

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

Texas A&M University

26. Stringfellow, Kendre. Immunomodulatory Effects of Probiotic and Anticoccidial Treatments in Broiler Chickens.

Degree: 2012, Texas A&M University

URL: http://hdl.handle.net/1969.1/ETD-TAMU-2012-08-11863

► Four experiments evaluated the impact of probiotic administration on the immune response of broilers vaccinated with a live coccidiosis vaccine. Experiment one showed that probiotic… (more)

▼ Four experiments evaluated the impact of probiotic administration on the immune response of broilers vaccinated with a live coccidiosis vaccine. Experiment one showed that probiotic administration increased heterophil and monocyte oxidative burst, and lymphocyte proliferation at multiple time points. In experiment two, probiotic + vaccine increased heterophil and monocyte oxidative burst on d 15 when compared with the negative controls. Overall, vaccine administration alone showed the highest response when compared to all other treatments. In the second trial, all birds were exposed to Eimeria oocysts in the litter and oral gavaged. The results showed that probiotic + vaccine resulted in greater heterophil and monocyte oxidative burst levels on d 14 and 28 when compared to the negative controls. Increases in lymphocyte proliferation were also seen in the probiotic + vaccine and probiotic alone broilers on d 14 among other treatments. In experiment three, heterophil oxidative burst was increased (p <= 0.05) in the vaccine alone group, vaccine with probiotic group, and the ionophore with probiotic group, when compared to the negative control. Monocyte oxidative burst was increased (p <= 0.05) in the vaccine with probiotic group on d 36 and 43, compared to the negative control. Lymphocyte proliferation was greater (p <= 0.05) on d 22 and 36 in the ionophore with probiotic group, when compared to the negative control. Experiment four showed that liver AVBD 2 gene expression elevated (p <= 0.05) in the probiotic + vaccine group relative to the probiotic alone group. Ileum AVBD 2 gene expression was not affected among any of the treatments was evaluated. Liver AVBD 9 was demonstrated to have higher (p <= 0.05) gene expression in the vaccine group when compared to controls. When AVBD 9 gene expression was evaluated in the ileum, a decrease (p <= 0.05) was observed in all treatments compared to the control group. These data suggest that simultaneous administration of probiotics during coccidiosis vaccination or ionophore treatment has the ability to modulate the immune response at varying time points. Advisors/Committee Members: Farnell, Morgan (advisor), Caldwell, David (committee member), Lee, Jason (committee member), Zhou, Huaijun (committee member).

Subjects/Keywords: Coccidiosis; Probiotic; Immunity; Defensin; Vaccine

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APA (6^th Edition):

Stringfellow, K. (2012). Immunomodulatory Effects of Probiotic and Anticoccidial Treatments in Broiler Chickens. (Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/ETD-TAMU-2012-08-11863

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):

Stringfellow, Kendre. “Immunomodulatory Effects of Probiotic and Anticoccidial Treatments in Broiler Chickens.” 2012. Thesis, Texas A&M University. Accessed February 25, 2020. http://hdl.handle.net/1969.1/ETD-TAMU-2012-08-11863.

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

MLA Handbook (7^th Edition):

Stringfellow, Kendre. “Immunomodulatory Effects of Probiotic and Anticoccidial Treatments in Broiler Chickens.” 2012. Web. 25 Feb 2020.

Vancouver:

Stringfellow K. Immunomodulatory Effects of Probiotic and Anticoccidial Treatments in Broiler Chickens. [Internet] [Thesis]. Texas A&M University; 2012. [cited 2020 Feb 25]. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-2012-08-11863.

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

Council of Science Editors:

Stringfellow K. Immunomodulatory Effects of Probiotic and Anticoccidial Treatments in Broiler Chickens. [Thesis]. Texas A&M University; 2012. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-2012-08-11863

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

27. Ramyar, Kasra Xerxes. Biochemical Characterization of Murine Qa-1.

Degree: 2014, Johns Hopkins University

URL: http://jhir.library.jhu.edu/handle/1774.2/37158

► Qa-1 is a member of the mouse MHC Ib family with roles in both the adaptive and innate arms of immunity. While it is presumed… (more)

Subjects/Keywords: Innate Immunity Immune Surveillance

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APA (6^th Edition):

Ramyar, K. X. (2014). Biochemical Characterization of Murine Qa-1. (Thesis). Johns Hopkins University. Retrieved from http://jhir.library.jhu.edu/handle/1774.2/37158

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):

Ramyar, Kasra Xerxes. “Biochemical Characterization of Murine Qa-1.” 2014. Thesis, Johns Hopkins University. Accessed February 25, 2020. http://jhir.library.jhu.edu/handle/1774.2/37158.

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

MLA Handbook (7^th Edition):

Ramyar, Kasra Xerxes. “Biochemical Characterization of Murine Qa-1.” 2014. Web. 25 Feb 2020.

Vancouver:

Ramyar KX. Biochemical Characterization of Murine Qa-1. [Internet] [Thesis]. Johns Hopkins University; 2014. [cited 2020 Feb 25]. Available from: http://jhir.library.jhu.edu/handle/1774.2/37158.

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

Council of Science Editors:

Ramyar KX. Biochemical Characterization of Murine Qa-1. [Thesis]. Johns Hopkins University; 2014. Available from: http://jhir.library.jhu.edu/handle/1774.2/37158

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

University of Hawaii – Manoa

28. Yang, Baojun. Cellular response of insect cells to virus infection.

Degree: 2015, University of Hawaii – Manoa

URL: http://hdl.handle.net/10125/100551

►

Ph.D. University of Hawaii at Manoa 2014.

RNA interference (RNAi) is the dsRNA-triggered gene regulatory mechanism that is evolutionally conserved in most eukaryotic cells. It… (more)

▼

Ph.D. University of Hawaii at Manoa 2014.

RNA interference (RNAi) is the dsRNA-triggered gene regulatory mechanism that is evolutionally conserved in most eukaryotic cells. It has been widely used as a powerful tool for functional genomics in various organisms. In flies, mosquitoes or other insect cells, gene functional analysis by RNAi is usually performed through introduced dsRNAs that are synthesized by in vitro transcription. RNAi serves as an important innate immunity against viruses in plants and invertebrates. It has recently been shown that Aedes albopictus mosquito C6/36 cells, commonly used for arbovirus propagation, possess an impaired RNAi pathway. In this study, we developed in vitro Dicer assay using extracts prepared from mosquito cells. Our results confirmed the inability of C6/36 cells to process dsRNAs into siRNAs, which is consistent with the loss-of-function of Dcr-2 due to a frameshift mutation. However, such a defect could not be complemented by introduction of Drosophila Dicer-2. To evaluate the RNAi-based antiviral mechanism in C6/36 cells, we analyzed the replication of a mutant Nodamura virus (NoV) genomic RNA1 of which viral RNAi suppressor B2 is not expressed (NoVR1ΔB2) and cannot accumulate to a detectable level in RNAi-competent cells. In C6/36 cells, the defective RNAi gives rise to complete restoration of NoVR1ΔB2 replication, suggesting that RNAi is the primary antiviral immunity in mosquito cells. At present, dsRNA, as the trigger of the antiviral RNAi pathway in invertebrate and plants, is the major efficiency limitation factor in RNAi. In this study, a plasmid-based system was developed to express dsRNA intracellular from a DNA cassette containing two convergent T7 promoters in Drosophila S2 cells. Efficient knockdown of a transiently expressed reporter gene or an endogenous gene can be achieved by dsRNA expressed from the system. A random cDNA library was constructed in the dsRNA expression cassette and initial screening led to identification of two host factors that are involved in antiviral response in Drosophila S2 cells. The plasmid-based dsRNA expression system provides an alternative tool for functional genomics in Drosophila and other insect cells.

Subjects/Keywords: Antiviral; dsRNA; RNAi; Innate Immunity

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

APA (6^th Edition):

Yang, B. (2015). Cellular response of insect cells to virus infection. (Thesis). University of Hawaii – Manoa. Retrieved from http://hdl.handle.net/10125/100551

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):

Yang, Baojun. “Cellular response of insect cells to virus infection.” 2015. Thesis, University of Hawaii – Manoa. Accessed February 25, 2020. http://hdl.handle.net/10125/100551.

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

MLA Handbook (7^th Edition):

Yang, Baojun. “Cellular response of insect cells to virus infection.” 2015. Web. 25 Feb 2020.

Vancouver:

Yang B. Cellular response of insect cells to virus infection. [Internet] [Thesis]. University of Hawaii – Manoa; 2015. [cited 2020 Feb 25]. Available from: http://hdl.handle.net/10125/100551.

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

Council of Science Editors:

Yang B. Cellular response of insect cells to virus infection. [Thesis]. University of Hawaii – Manoa; 2015. Available from: http://hdl.handle.net/10125/100551

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

University of Minnesota

29. LaRue, Rebecca St. Claire. Dynamics of the mammalian APOBEC3 locus and the relationship between mammalian APOBEC3 and Lentiviral Vif proteins.

Degree: Comparative and Molecular Biosciences, 2010, University of Minnesota

URL: http://purl.umn.edu/97083

► The mammalian immune system must be dynamic in the face of a diverse and ever-changing array of pathogens. Successful pathogens have evolved to overcome host… (more)

▼ The mammalian immune system must be dynamic in the face of a diverse and ever-changing array of pathogens. Successful pathogens have evolved to overcome host immunity. One of the most successful pathogens in the last century is the human immunodeficiency virus (HIV), which is the etiological agent responsible for the global acquired immune deficiency syndrome (AIDS) epidemic. Currently, one of the most studied host-pathogen interactions is between the cellular anti-retroviral APOBEC3 (A3) proteins and HIV viral infectivity factor (Vif) protein. A3 proteins are cytosine deaminases that primarily inhibit retroviruses and retrotransposons by mutating cytosines to uracils in retroviral DNA during reverse transcription. When HIV Vif is present, it can bind to certain A3 proteins and recruit cellular degradation complexes to target these anti-retroviral proteins for proteasomal degradation. HIV-like viruses (lentiviruses) infect other mammals and are the inspiration for studying A3 proteins in other mammals. The ultimate goal of this comparative study was to gain a better understanding of how the lentiviral Vif protein counteracts host A3 proteins. The first component of this dissertation is dedicated to the process of determining the complete A3 protein repertoires of cow and sheep (representatives of the artiodactyl lineage), which are both infected with a lentiviruses. The second component of this dissertation was to test if these artiodactyl A3 proteins were functional. Cow and sheep A3 proteins demonstrate intrinsic DNA cytosine deaminase activity and localize in cells similar to human A3 proteins. Furthermore, certain cow A3 proteins are capable of restricting HIV and are neutralized in the presence of cattle-specific lentiviral Vif (bovine immunodeficiency virus). The last component of this dissertation, a panel of conserved mammalian A3 proteins were tested to determine if each A3 protein interacts specifically with its species lentiviral Vif protein. It was shown that each representative host A3 protein is degraded in the presence of its species specific lentiviral Vif, suggesting a conserved interaction between mammalian A3 proteins and their species specific lentiviral Vif protein.

Subjects/Keywords: APOBEC3; Comparative; HIV; Immunity; Lentivirus

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

APA (6^th Edition):

LaRue, R. S. C. (2010). Dynamics of the mammalian APOBEC3 locus and the relationship between mammalian APOBEC3 and Lentiviral Vif proteins. (Thesis). University of Minnesota. Retrieved from http://purl.umn.edu/97083

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):

LaRue, Rebecca St Claire. “Dynamics of the mammalian APOBEC3 locus and the relationship between mammalian APOBEC3 and Lentiviral Vif proteins.” 2010. Thesis, University of Minnesota. Accessed February 25, 2020. http://purl.umn.edu/97083.

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

MLA Handbook (7^th Edition):

LaRue, Rebecca St Claire. “Dynamics of the mammalian APOBEC3 locus and the relationship between mammalian APOBEC3 and Lentiviral Vif proteins.” 2010. Web. 25 Feb 2020.

Vancouver:

LaRue RSC. Dynamics of the mammalian APOBEC3 locus and the relationship between mammalian APOBEC3 and Lentiviral Vif proteins. [Internet] [Thesis]. University of Minnesota; 2010. [cited 2020 Feb 25]. Available from: http://purl.umn.edu/97083.

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

Council of Science Editors:

LaRue RSC. Dynamics of the mammalian APOBEC3 locus and the relationship between mammalian APOBEC3 and Lentiviral Vif proteins. [Thesis]. University of Minnesota; 2010. Available from: http://purl.umn.edu/97083

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

University of Rochester

30. Aggrey, Angela Akosua. A Novel Protective Role for Platelet-Mediated Immune Responses in Murine Experimental Cerebral Malaria.

Degree: PhD, 2013, University of Rochester

URL: http://hdl.handle.net/1802/27239

► Cerebral malaria is caused by complications from Plasmodium falciparum infection and claims hundreds of thousands of lives of young children in endemic countries annually. Platelets… (more)

Subjects/Keywords: Platelets; Innate Immunity, Malaria; Inflammation

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

APA (6^th Edition):

Aggrey, A. A. (2013). A Novel Protective Role for Platelet-Mediated Immune Responses in Murine Experimental Cerebral Malaria. (Doctoral Dissertation). University of Rochester. Retrieved from http://hdl.handle.net/1802/27239

Chicago Manual of Style (16^th Edition):

Aggrey, Angela Akosua. “A Novel Protective Role for Platelet-Mediated Immune Responses in Murine Experimental Cerebral Malaria.” 2013. Doctoral Dissertation, University of Rochester. Accessed February 25, 2020. http://hdl.handle.net/1802/27239.

MLA Handbook (7^th Edition):

Aggrey, Angela Akosua. “A Novel Protective Role for Platelet-Mediated Immune Responses in Murine Experimental Cerebral Malaria.” 2013. Web. 25 Feb 2020.

Vancouver:

Aggrey AA. A Novel Protective Role for Platelet-Mediated Immune Responses in Murine Experimental Cerebral Malaria. [Internet] [Doctoral dissertation]. University of Rochester; 2013. [cited 2020 Feb 25]. Available from: http://hdl.handle.net/1802/27239.

Council of Science Editors:

Aggrey AA. A Novel Protective Role for Platelet-Mediated Immune Responses in Murine Experimental Cerebral Malaria. [Doctoral Dissertation]. University of Rochester; 2013. Available from: http://hdl.handle.net/1802/27239

Open Access Theses and Dissertations