Thesis (M.Sc.)--University of Alberta, 2010. / A thesis submitted to the Faculty of Graduate Studies and Research in partial fulfillment of the requirements for the degree of Master of Science in Experimental Medicine, Department of Medicine. Title from pdf file main screen (viewed on April 24 2010). Includes bibliographical references.

Thesis (Ph.D.)--University of Alberta, 2010. / A thesis submitted to the Faculty of Graduate Studies and Research in partial fulfillment of the requirements for the degree of Doctor of Philosophy, Department of Medical Microbiology and Immunology. Title from pdf file main screen (viewed on April 24, 2010). Includes bibliographical references.

Thesis (Ph. D.)--Ohio State University, 2006. / Available online via OhioLINK's ETD Center; full text release delayed at author's request until 2009 Apr 26

Thesis (Ph.D.)--Memorial University of Newfoundland, 2004. / Includes bibliographical references.

Thesis (doctoral)--University of Lund, 1996. / Added t.p. with thesis statement added.

Thesis (Ph. D.)--Illinois State University, 1994. / Title from title page screen, viewed March 21, 2006. Dissertation Committee: H. Tak Cheung (chair), Herman E. Brockman, Lynne A. Lucher, Philip D. Morse, Anthony J. Otsuka. Includes bibliographical references (leaves 101-111) and abstract. Also available in print.

Thesis (Ph. D.)--Ohio State University, 2007. / Full text release at OhioLINK's ETD Center delayed at author's request

IL-33 is a pleiotropic cytokine that orchestrates both innate and adaptive immunity. It is commonly associated with type 2 immune responses but recently expression of the IL-33 receptor, ST2, was reported on Treg cells found preferentially in non-lymphoid tissues, such as the visceral adipose tissue, muscle or colon. A crucial role of Tregs in maintaining intestinal homeostasis has been well described. However, little is known about the functional relevance of the ST2-expressing Treg population in the colon. Phenotypic and functional characterisation of Tregs in the gut revealed the presence of two distinct populations: ST2⁺/Gata3⁺ and Rorγt⁺ Tregs. Thymic-derived ST2⁺/Gata3⁺ Tregs showed a more activated phenotype and produced IL-10 under homeostatic conditions. Upon microbial challenge and colitis, ST2+/Gata3+ Tregs were decreased, while Rorγt⁺ Tregs expanded. Furthermore, in vitro experiments demonstrated that IL-33 directly induced activation of the Gata3 pathway in Tregs, which enhanced expression of Foxp3 and ST2. Additionally, amphiregulin was also induced in Tregs upon stimulation with IL-33. However, in vivo, IL-33 was dispensable for both the maintenance of Treg cells under homeostatic conditions and Treg function in Helicobacter hepaticus-driven colitis. Investigation of the negative regulators of IL-33 showed that IL-23 inhibited IL-33-mediated effects on Tregs. We also observed increased production of soluble ST2 by stromal cells during intestinal inflammation, which likely contributed to the reduction of IL-33 bioavailability. Finally, a systematic analysis of the cellular source of IL-33 revealed that PDGRFα⁺ stromal cells located in the T cell zone of secondary and tertiary lymphoid tissues were a major IL-33-producing cell population in the gut. Collectively, our findings suggest that signals received by the stromal compartment upon cell injury may trigger a specific phenotype of Tregs with a repair capacity, and thus, promote intestinal homeostasis. These findings improve our understanding of tissue-resident Tregs and open an exciting avenue to explore heterocellular signalling between stromal cells and Tregs.

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Objective: The survival rates for cardiac arrest patients to hospital discharge are very low. Post-arrest patients have an immune response and usually a period of immunosuppression. When CD3+ T cells activate, they switch from primarily relying on aerobic metabolism to primarily relying on anaerobic metabolism. The goal of this study is to characterize the immune system of post-cardiac arrest patients. The specific objectives are (1) to determine the time period after the occurrence of a cardiac arrest that a patient acquires an infection, (2) to identify the most common types of infections in post-arrest patients, (3) to compare in vitro the cellular oxygen consumption of immune cells post-cardiac arrest with healthy controls, and (4) to compare cell proliferation and ATP production of immune cells post-cardiac arrest with healthy controls. Methods: We conducted a retrospective chart review of 170 cardiac arrest patients (Beth Israel Deaconess Medical Center) who had return of spontaneous circulation. We measured oxygen consumption rates of peripheral blood mononuclear cells (PBMCs) in cardiac arrest patients and healthy controls. We also measured cell proliferation and ATP production of CD3+ T cells in cardiac arrest patients and healthy controls. Results: Of the 170 cardiac arrest patients we reviewed, 42% had at least one incidence of infection. The length of time from cardiac arrest to first positive culture was 4 days, with pneumonia and urinary tract infections the most common diagnoses. The PBMCs of cardiac arrest patients showed a significant decrease in oxygen consumption post arrest compared with healthy controls. When thiamine was added to the PBMC samples of cardiac arrest patients, there was a significant increase in oxygen consumption from baseline. There was no significant difference in cell proliferation or ATP production of CD3+ T cells between the two groups of post-cardiac arrest patients and healthy controls. Conclusion: Many patients suffer from infections post-cardiac arrest, and future research is needed on this subject. Our data support the hypothesis that post-arrest patients have a period of hyperimmune response followed by a period of immunosuppression.