Current Diabetes Reports

, 14:518

Interleukin-7 and Type 1 Diabetes

Authors

    • Diabetes Research Institute (DRI)IRCCS San Raffaele Scientific Institute
  • Ezio Bonifacio
    • DFG-Center for Regenerative Therapies DresdenTechnische Universität Dresden
Pathogenesis of Type 1 Diabetes (A Pugliese, Section Editor)

DOI: 10.1007/s11892-014-0518-9

Cite this article as:
Monti, P. & Bonifacio, E. Curr Diab Rep (2014) 14: 518. doi:10.1007/s11892-014-0518-9
Part of the following topical collections:
  1. Topical Collection on Pathogenesis of Type 1 Diabetes

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.

Keywords

Type 1 diabetesInterleukin-7IL-7IL-7 receptorSoluble IL-7RαsCD127Homeostatic proliferationT-cells

Copyright information

© Springer Science+Business Media New York 2014