Interferon-alpha as a mediator of polyinosinic:polycytidylic acid-induced type 1 diabetes.

Abstract : A number of studies and clinical case reports have implicated interferon (IFN)-alpha as a potential mediator of type 1 diabetes pathogenesis. Administration of polyinosinic:polycytidylic acid (poly I:C), a mimic of viral double-stranded RNA, induces diabetes in C57BL/6 mice expressing the B7.1 costimulatory molecule in islets. We investigated the potential role of IFN-alpha in this disease model. The quantitative correlation between IFN-alpha levels and time to diabetes, diabetes prevention with anti-IFN-alpha antibody, and ability of IFN-alpha itself to induce diabetes are consistent with the hypothesis that poly I:C in this model acts by induction of IFN-alpha in a genetically susceptible host. Numerous recent studies highlight the importance of the innate immune system and toll receptors in determining adaptive immune responses, and we speculate that for type 1 diabetes, viral and other environmental factors may act through induction of IFNs.
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Devasenan Devendra, Jean Jasinski, Evie Melanitou, Maki Nakayama, Marcella Li, et al.. Interferon-alpha as a mediator of polyinosinic:polycytidylic acid-induced type 1 diabetes.. Diabetes, American Diabetes Association, 2005, 54 (9), pp.2549-56. 〈10.2337/diabetes.54.9.2549〉. 〈pasteur-01643740〉



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