Central role for interleukin-2 in type 1 diabetes

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Abstract

Type 1 diabetes presents clinically with overt hyperglycemia resulting from progressive immune-mediated destruction of pancreatic β-cells and associated metabolic dysfunction. Combined genetic and immunological studies now highlight deficiencies in both the interleukin-2 (IL-2) receptor and its downstream signaling pathway as a central defect in the pathogenesis of type 1 diabetes. Prior intervention studies in animal models indicate that augmenting IL-2 signaling can prevent and reverse disease, with protection conferred primarily by restoration of regulatory T-cell (Treg) function. In this article, we will focus on studies of type 1 diabetes noting deficient IL-2 signaling and build what we believe forms the molecular framework for their contribution to the disease. This activity results in the identification of a series of potentially novel therapeutic targets that could restore proper immune regulation in type 1 diabetes by augmenting the IL-2 pathway. © 2012 by the American Diabetes Association.

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Hulme, M. A., Wasserfall, C. H., Atkinson, M. A., & Brusko, T. M. (2012, January). Central role for interleukin-2 in type 1 diabetes. Diabetes. https://doi.org/10.2337/db11-1213

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