title: Interleukin-7 and 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.
authors.affiliation: Diabetes Research Institute (DRI), IRCCS San Raffaele Scientific Institute, Via Olgettina 60, 20132, Milan, Italy, paolo.monti@hsr.it.
authors.forename: Paolo
authors.initials: P
authors.lastname: Monti
authors.forename: Ezio
authors.initials: E
authors.lastname: Bonifacio
mesh_terms: D000818:Animals; D015551:Autoimmunity / Q000276:immunology; D003922:Diabetes Mellitus, Type 1 / Q000276:immunology*; D006801:Humans; D015851:Interleukin-7 / Q000378:metabolism*; D008213:Lymphocyte Activation / Q000276:immunology; D020395:Receptors, Interleukin-7 / Q000378:metabolism; D013601:T-Lymphocytes / Q000276:immunology
chemical_list: D015851:Interleukin-7; D020395:Receptors, Interleukin-7