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Complement C3 deficiency prevent against the onset of streptozotocin-induced autoimmune diabetes involving expansion of regulatory T cells
- Source :
-
Clinical Immunology . Sep2011, Vol. 140 Issue 3, p236-243. 8p. - Publication Year :
- 2011
-
Abstract
- Abstract: Recent studies have demonstrated that complement contributes to the development of autoimmune diabetes. However, the mechanisms remain unknown. Herein, using a model of streptozotocin (STZ)-induced diabetes, we found the presence of immune tolerance to self islet in complement C3-deficient mice after STZ. Higher number of CD4+CD25+ regulatory T cells (Tregs) with characteristics of expressing Foxp3 was observed in C3−/− mice. These C3−/− Tregs exhibited enhanced suppressive capacity to effector cell proliferation. The central role of Tregs was further evidenced by that depleting these cells using anti-CD25 antibody dramatically abrogated the preventive effects of C3 deficiency on STZ-induced diabetes. Importantly, transforming growth factor-β (TGF-β) was a key factor for Treg-mediated immune suppression as blocking TGF-β activity reversed suppressive capacity of Tregs in vitro and diabetes-resistant effects of C3 deficiency in vivo. These findings suggest that resistance to overt diabetes in STZ-treated C3−/− mice involves a population of Tregs in TGF-β-dependent manner. [Copyright &y& Elsevier]
Details
- Language :
- English
- ISSN :
- 15216616
- Volume :
- 140
- Issue :
- 3
- Database :
- Academic Search Index
- Journal :
- Clinical Immunology
- Publication Type :
- Academic Journal
- Accession number :
- 64885134
- Full Text :
- https://doi.org/10.1016/j.clim.2011.02.004