Journal article
Defects in the Bcl-2-regulated apoptotic pathway lead to preferential increase of CD25lowFoxp3 anergic CD4 T cells
Y Zhan, Y Zhang, D Gray, EM Carrington, P Bouillet, HJ Ko, L O'Reilly, IP Wicks, A Strasser, AM Lew
Journal of Immunology | AMER ASSOC IMMUNOLOGISTS | Published : 2011
Abstract
Defects in the Bcl-2-regulated apoptotic pathway inhibit the deletion of self-reactive T cells. What is unresolved, however, is the nature and fate of such self-reactive T cells escaping deletion. In this study, we report that mice with such defects contained increased numbers of CD25lowFoxp3+ cells in the thymus and peripheral lymph tissues. The increased CD25lowFoxp3+ population contained a large fraction of cells bearing self-reactive TCRs, evident from a prominent increase in self-superantigen-specific Foxp3+Vβ5+CD4+ T cells in BALB/c Bim-/- mice compared with control animals. The survival rate of the expanded CD25lowFoxp3+ cells was similar to that of CD25highFoxp3+ CD4 T cells in vitro..
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Grants
Awarded by National Cancer Institute
Funding Acknowledgements
This work was supported by National Health and Medical Research Council of Australia Program Grants 516700 and 461221, Project Grants 575543 and 637324, National Health and Medical Research Council Australia Fellowship 461299, National Health and Medical Research Council Career Development Awards 516754 and 637353, National Health and Medical Research Council Independent Research Institutes Infrastructure Support Scheme Grant 361646, the National Institutes of Health (CA 043540), the Leukemia and Lymphoma Society (LLS SCOR 7413), Juvenile Diabetes Research Foundation Grant 466658, and a Victorian State Government Operational Infrastructure Support grant.