کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
3257236 1589431 2011 8 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Complement C3 deficiency prevent against the onset of streptozotocin-induced autoimmune diabetes involving expansion of regulatory T cells
موضوعات مرتبط
علوم زیستی و بیوفناوری ایمنی شناسی و میکروب شناسی ایمونولوژی
پیش نمایش صفحه اول مقاله
Complement C3 deficiency prevent against the onset of streptozotocin-induced autoimmune diabetes involving expansion of regulatory T cells
چکیده انگلیسی

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.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Clinical Immunology - Volume 140, Issue 3, September 2011, Pages 236–243
نویسندگان
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