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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 Foxp3was observed in C3-/-mice.These C3-/-Tregs exhibited enhanced suppressive capacity to effector cell proliferation.