Interleukin-7 and type 1 diabetes

Paolo Monti, Ezio Bonifacio

Research output: Contribution to journalArticle

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.

Original languageEnglish
Article number518
JournalCurrent Diabetes Reports
Volume14
Issue number9
DOIs
Publication statusPublished - 2014

Keywords

  • Homeostatic proliferation
  • IL-7
  • IL-7 receptor
  • Interleukin-7
  • SCD127
  • Soluble IL-7Rα
  • T-cells
  • Type 1 diabetes

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Internal Medicine
  • Medicine(all)

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