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B cell modulation by toxic shock syndrome toxin-1 induced CD4⁺ regulatory T cells generated in BALB/c mice

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Title: B cell modulation by toxic shock syndrome toxin-1 induced CD4⁺ regulatory T cells generated in BALB/c mice
Author: Lam, Grace
Degree: Master of Science - MSc
Program: Experimental Medicine
Copyright Date: 2006
Issue Date: 2010-01-16
Series/Report no. UBC Retrospective Theses Digitization Project [http://www.library.ubc.ca/archives/retro_theses/]
Abstract: Among the most exciting recent advances in the field of immunology is research on the regulatory T cells. Tregs, comprising only 5-10% of the peripheral CD4+ T cell population, are known to suppress T cell function. One type of Tregs is the antigen induced Tregs, which can be generated in mice following repeated subcutaneous injections of Toxic Shock Syndrome Toxin- 1, a superantigen secreted by the bacteria, Staphylococcus aureus. These Tregs have been shown to have the ability to down regulate T cell activity and proliferation via the secretion of cytokines (IL-10 and TGF-β). Recent findings suggest that Tregs cells not only control T cell activity but B cell activity as well. In this study, the ability of these TSST-1 induced Tregs to modulate B cell proliferation, viability and antibody production is explored. It was found that the adoptive transfer of TSST-1 primed CD4+ T cells into mice hyperimmunized with TNP-KLH suppressed TNP-specific antibody production while PBS primed CD4+ T cells did not. The effect of CD4+CD25+ versus CD4+CD25- T cells was further investigated in vitro. Co-culturing B cells with PBS primed CD4+CD25+ or CD4+CD25- T cells in the presence of 1 nM TSST-1 caused B cells to undergo multiple cycles of proliferation. The PBS primed CD25+ T cell population induced a Th1-like response (IgG2a production) while the PBS primed CD25- T cells induced a Th2-like response (IgG1 production). In contrast, co-culturing B cells with either TSST-1 primed CD4+CD25+ or CD4+CD25- T cells suppressed B cell proliferation and function but through entirely different mechanisms. TSST-1 primed CD4+CD25+ Tregs prevented B cell proliferation by inducing B cell apoptosis, while TSST-1 primed CD4+CD25- Tregs temporally suppressed the onset of a Th2-like response. B cell suppression appeared to be mediated by both the secretion of IL-10 and TGF-β and by cell-to-cell mediated mechanisms. These data provide evidence that in addition to modulating T cell activity, TSST-1 induced Tregs also regulate B cell activity both in vitro and in vivo, thus raising the possibility of using TSST-1 primed Tregs for controlling both T and B cell-mediated autoimmune diseases.
Affiliation: Medicine, Faculty of
URI: http://hdl.handle.net/2429/18331
Scholarly Level: Graduate

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