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J Biol Chem. 2007 May 25;282(21):15325-9. Epub 2007 Mar 29.

Triggering the innate antiviral response through IRF-3 activation.

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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-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.

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