| First Author | Gao X | Year | 2011 |
| Journal | Clin Immunol | Volume | 140 |
| Issue | 3 | Pages | 236-43 |
| PubMed ID | 21767994 | Mgi Jnum | J:177207 |
| Mgi Id | MGI:5294494 | Doi | 10.1016/j.clim.2011.02.004 |
| Citation | Gao X, et al. (2011) Complement C3 deficiency prevent against the onset of streptozotocin-induced autoimmune diabetes involving expansion of regulatory T cells. Clin Immunol 140(3):236-43 |
| abstractText | 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-beta (TGF-beta) was a key factor for Treg-mediated immune suppression as blocking TGF-beta 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-beta-dependent manner. |
