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J. Biol. Chem., Vol. 282, Issue 21, 15325-15329, May 25, 2007
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Minireview
Triggering the Innate Antiviral Response through IRF-3 Activation*
From the Lady Davis Institute for Medical Research-Jewish General Hospital, Departments of Microbiology & Immunology, Medicine, and Oncology, McGill University, Montreal H3T 1E2, Canada
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-
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.
* This minireview will be reprinted in the 2007 Minireview Compendium, which will be available in January, 2008. This research was supported by grants from the Canadian Institutes of Health Research (CIHR), the National Cancer Institute of Canada, with the support of the Canadian Cancer Society, and CANFAR, the Canadian Foundation for AIDS Research. This is the third article of three in the Innate Immunity Minireview Series.
1 Supported by a CIHR Senior Investigator award. To whom correspondence should be addressed. E-mail: john.hiscott{at}mcgill.ca.
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