Adaptive Islet-Specific Regulatory CD4 T Cells Control Autoimmune Diabetes and Mediate the Disappearance of Pathogenic Th1 Cells In Vivo

摘要: Adaptive regulatory T cells that develop from naive CD4 in response to exposure Ag can act as immunotherapeutic agents control immune responses. We show effectors generated murine islet-specific by TCR stimulation with IL-2 and TGF-beta1 have potent suppressive activity. They prevent spontaneous development of type 1 diabetes NOD mice inhibit pancreatic infiltrates disease onset orchestrated Th1 effectors. These do not require innate CD25+ for generation or function, nor they share some characteristics typically associated them, including expression CD25. However, the adaptive population does acquire X-linked forkhead/winged helix transcription factor, FoxP3, which is cell function maintains vivo. One mechanism may via FasL-dependent cytotoxicity, occurs vitro. In vivo, eliminate lymphoid tissues, where Fas/FasL interactions potentially play a role because persist when this pathway blocked. The results suggest part impairing survival cells, thereby inhibiting localization autoaggressive islets.