Triggering the innate antiviral response through IRF-3 activation

被引:382
作者
Hiscott, John [1 ]
机构
[1] Jewish Gen Hosp, Lady Davis Inst Med Res, Dept Microbiol & Immunol, Montreal, PQ H3T 1E2, Canada
[2] McGill Univ, Dept Oncol, Montreal, PQ H3T 1E2, Canada
[3] McGill Univ, Dept Med, Montreal, PQ H3T 1E2, Canada
关键词
D O I
10.1074/jbc.R700002200
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Rapid induction of type I interferon (IFN) expression is a central event in the establishment of the innate immune response against viral infection and requires the activation of multiple transcriptional proteins following engagement and signaling through Toll-like receptor-dependent and -independent pathways. The transcription factor interferon regulatory factor-3 (IRF-3) contributes to a first line of defense against viral infection by inducing the production of IFN-beta that in turn amplifies the IFN response and the development of antiviral activity. In murine knock-out models, the absence of IRF-3 and the closely related IRF-7 ablates IFN production and increases viral pathogenesis, thus supporting a pivotal role for IRF-3/IRF-7 in the development of the host antiviral response.
引用
收藏
页码:15325 / 15329
页数:5
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