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Curr Diab Rep. 2014;14(9):518. doi: 10.1007/s11892-014-0518-9.

Interleukin-7 and type 1 diabetes.

Author information

1
Diabetes Research Institute (DRI), IRCCS San Raffaele Scientific Institute, Via Olgettina 60, 20132, Milan, Italy, paolo.monti@hsr.it.

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.

PMID:
24996523
DOI:
10.1007/s11892-014-0518-9
[Indexed for MEDLINE]

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