IRF3 inhibits nuclear translocation of NF-κB to prevent viral inflammation.

ABSTRACT: Interferon (IFN) regulatory factor 3 (IRF3) is a transcription factor activated by phosphorylation in the cytoplasm of a virus-infected cell; by translocating to the nucleus, it induces transcription of IFN-β and other antiviral genes. We have previously reported IRF3 can also be activated, as a proapoptotic factor, by its linear polyubiquitination mediated by the RIG-I pathway. Both transcriptional and apoptotic functions of IRF3 contribute to its antiviral effect. Here, we report a nontranscriptional function of IRF3, namely, the repression of IRF3-mediated NF-κB activity (RIKA), which attenuated viral activation of NF-κB and the resultant inflammatory gene induction. In Irf3^-/- mice, consequently, Sendai virus infection caused enhanced inflammation in the lungs. Mechan

SUBMITTER: Popli S 

PROVIDER: S-EPMC9478676 | biostudies-literature | 2022 Sep

REPOSITORIES: biostudies-literature