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Central Role for Interleukin-2 in Type 1 Diabetes
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Central Role for Interleukin-2 in Type 1 Diabetes
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Journal Article
Central Role for Interleukin-2 in Type 1 Diabetes
2012
Overview
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.
Publisher
American Diabetes Association
Subject
/ Biological and medical sciences
/ Cells
/ Cellular signal transduction
/ Complications and side effects
/ Diabetes
/ Diabetes Mellitus, Type 1 - etiology
/ Diabetes Mellitus, Type 1 - genetics
/ Diabetes Mellitus, Type 1 - metabolism
/ Diabetes. Impaired glucose tolerance
/ Endocrine pancreas. Apud cells (diseases)
/ Etiopathogenesis. Screening. Investigations. Target tissue resistance
/ Genetic Predisposition to Disease
/ Humans
/ Kinases
/ Receptors, Interleukin-2 - chemistry
/ Receptors, Interleukin-2 - genetics
/ Receptors, Interleukin-2 - metabolism
/ Receptors, Interleukin-2 - physiology
