Redox-Sensitive Innate Immune Pathways During Macrophage Activation in Type 1 Diabetes

摘要

Significance: Type 1 diabetes (T1D) is an autoimmune disease resulting in beta-cell destruction mediated by islet-infiltrating leukocytes. The role of oxidative stress in human and murine models of T1D is highly significant as these noxious molecules contribute to diabetic complications and beta-cell lysis, but their direct impact on dysregulated autoimmune responses is highly understudied. Pro-inflammatory macrophages play a vital role in the initiation and effector phases of T1D by producing free radicals and pro-inflammatory cytokines to facilitate beta-cell destruction and to present antigen to autoreactive T cells