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Interleukin-7 and Type 1 Diabetes

  • Pathogenesis of Type 1 Diabetes (A Pugliese, Section Editor)
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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.

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Paolo Monti and Ezio Bonifacio declare that they have no conflict of interest.

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This article does not contain any studies with human or animal subjects performed by any of the authors.

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Correspondence to Paolo Monti.

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

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Monti, P., Bonifacio, E. Interleukin-7 and Type 1 Diabetes. Curr Diab Rep 14, 518 (2014). https://doi.org/10.1007/s11892-014-0518-9

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