Anti-Inflammatory Therapy in Type 1 Diabetes

Type 1 diabetes (T1D) is a multi-factorial, organ-specific autoimmune disease in genetically susceptible individuals, which is characterized by a selective and progressive loss of insulin-producing beta-cells. Cells mediating innate as well as adaptive immunity infiltrate pancreatic islets, thereby generating an aberrant inflammatory process called insulitis that can be mirrored by a pathologic autoantibody production and autoreactive T-cells. In tight cooperation with infiltrating innate immune cells, which secrete high levels of pro-inflammatory cytokines like IL-1 beta, TNF alpha, and INF gamma effector T-cells trigger the fatal destruction process of beta-cells. There is ongoing discussion on the contribution of inflammation in T1D pathogenesis, ranging from a bystander reaction of autoimmunity to a dysregulation of immune responses that initiate inflammatory processes and thereby actively promoting beta-cell death. Here, we review recent advances in anti-inflammatory interventions in T1D animal models and preclinical studies and discuss their mode of action as well as their capacity to interfere with T1D development.