, 14:518
Date: 05 Jul 2014

Interleukin-7 and Type 1 Diabetes

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Abstract

Antigen-experienced T-cells directly target and destroy insulin-producing beta cells in patients with Type 1 diabetes. Consequently, T-cells are also major targets of immunomodulatory strategies that aim to prevent or delay the immune mediated loss of islet beta-cell function. These strategies have had modest success, prompting efforts into better defining the mechanisms that drive the differentiation of quiescent autoreactive clones into pathogenic effector and memory T-cells. Recent and novel findings now indicate that in addition to the classic mechanisms of antigenic recognition, autoreactive T-cell differentiation and expansion can be boosted by the homeostatic cytokine interleukin-7. In this article, we discuss recent evidence of the role of IL-7 mediated T-cell proliferation in the pathogenesis of Type 1 diabetes and the rationale for including immunomodulatory molecules targeting the IL-7/IL-7R axis in immunotherapeutic strategies to control beta-cell autoimmunity.

This article is part of the Topical Collection on Pathogenesis of Type 1 Diabetes