| First Author | Devendra D | Year | 2005 |
| Journal | Diabetes | Volume | 54 |
| Issue | 9 | Pages | 2549-56 |
| PubMed ID | 16123342 | Mgi Jnum | J:129147 |
| Mgi Id | MGI:3768739 | Doi | 10.2337/diabetes.54.9.2549 |
| Citation | Devendra D, et al. (2005) Interferon-alpha as a mediator of polyinosinic:polycytidylic acid-induced type 1 diabetes. Diabetes 54(9):2549-56 |
| abstractText | 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. |
