Triggering the innate antiviral response through IRF-3 activation.
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.
Hiscott
John
J
Lady Davis Institute for Medical Research-Jewish General Hospital, Departments of Microbiology & Immunology, Medicine, and Oncology, McGill University, Montreal H3T 1E2, Canada. john.hiscott@mcgill.ca
D000818:Animals; D006801:Humans; D007113:Immunity, Innate / Q000502:physiology*; D050838:Interferon Regulatory Factor-3 / Q000276:immunology*; D050839:Interferon Regulatory Factor-7 / Q000276:immunology; D007370:Interferon Type I / Q000276:immunology*; D015398:Signal Transduction / Q000276:immunology*; D014777:Virus Diseases / Q000276:immunology*; D014780:Viruses / Q000276:immunology*
D050838:Interferon Regulatory Factor-3; D050839:Interferon Regulatory Factor-7; D007370:Interferon Type I