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

被引：48

作者：

Devendra, D ^{[1
]}

Jasinski, J ^{[1
]}

Melanitou, E ^{[1
]}

Nakayama, M ^{[1
]}

Li, M ^{[1
]}

Hensley, B ^{[1
]}

Paronen, J ^{[1
]}

Moriyama, H ^{[1
]}

Miao, DM ^{[1
]}

Eisenbarth, GS ^{[1
]}

Liu, E ^{[1
]}

机构：

[1] Univ Colorado, Hlth Sci Ctr, Barbara Davis Ctr Childhood Diabet, Denver, CO 80262 USA

来源：

DIABETES | 2005年 / 54卷 / 09期

关键词：

D O I：

10.2337/diabetes.54.9.2549

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

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.

引用

页码：2549 / 2556

页数：8

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