Complement C3 deficiency prevent against the onset of streptozotocin-induced autoimmune diabetes involving expansion of regulatory T cells

摘要: Abstract Recent studies have demonstrated that complement contributes to the development of autoimmune diabetes. However, mechanisms remain unknown. Herein, using a model streptozotocin (STZ)-induced diabetes, we found presence immune tolerance self islet in C3-deficient mice after STZ. Higher number CD4 + CD25+ regulatory T cells (Tregs) with characteristics expressing Foxp3 was observed C3−/− mice. These Tregs exhibited enhanced suppressive capacity effector cell proliferation. The central role further evidenced by depleting these anti-CD25 antibody dramatically abrogated preventive effects C3 deficiency on STZ-induced Importantly, transforming growth factor-β (TGF-β) key factor for Treg-mediated suppression as blocking TGF-β activity reversed vitro and diabetes-resistant vivo. findings suggest resistance overt diabetes STZ-treated involves population TGF-β-dependent manner.