Journal
DIABETES
Volume 54, Issue 9, Pages 2549-2556Publisher
AMER DIABETES ASSOC
DOI: 10.2337/diabetes.54.9.2549
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Funding
- NIAID NIH HHS [AI 050864, AI 055466] Funding Source: Medline
- NIDDK NIH HHS [DK 055969, P30 DK57516, DK 062718, DK 06405] Funding Source: Medline
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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 I diabetes, viral and other environmental factors may act through induction of IFNs.
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