Abstract
Type 1 diabetes (T1D) is a multi-factorial, organspecific autoimmune disease in genetically susceptible individuals, which is characterized by a selective and progressive loss of insulin-producing β-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-1β, TNFα, and INFγ effector T-cells trigger the fatal destruction process of β-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 β-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. © Springer Science+Business Media, LLC 2012.
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Baumann, B., Salem, H. H., & Boehm, B. O. (2012). Anti-inflammatory therapy in type 1 diabetes. Current Diabetes Reports, 12(5), 499–509. https://doi.org/10.1007/s11892-012-0299-y
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