Increased level of type I Interferon (IFN) during type I diabetes (T1D) induces apoptosis in spleen-homing T cells

摘要: Type I diabetes (TID) is an autoimmune disease characterized by abnormalities in the defense mechanisms against a variety of infectious agents. Susceptibility to infections occurring diabetic individuals attributed decrease number lymphocytes, which probably clinical consequence occurrence apoptosis described diabetes. TID associated with increased cytokines that dampen lymphocytes proliferation, functions and subsequently increase risk infection. Previous studies have reported IFN-α level pathogenesis. In present study, we further investigated effect blocking type IFN receptor signaling pathway on lymphocyte proliferation within spleen as secondary lymphoid organ streptozotocin (STZ)-induced mouse model. Three groups mice were used (10 each group): group 1, control non-diabetic mice; 2, 3, intraperitoneal injected anti-IFNAR1 mg/kg body weight once/day for up 20 days). We found exhibited apoptosis, DNA fragmentation, chromatin condensation cell shrinkage; prolonged elevation TNF-α levels obvious reduction spleen-homing T compared mice. Interestingly, significantly decreased (P< 0.05) apoptotic changes lymphocyte, restored distribution numbers also non treated Our data revealed correlation between elevated during perturbation architecture organs.