Nuclear factor ?B2 p52 protein has a role in antiviral immunity through I?B kinase epsilon-dependent induction of Sp1 protein and interleukin 15.

ABSTRACT: In this study we describe a previously unreported function for NF?B2, an NF?B family transcription factor, in antiviral immunity. NF?B2 is induced in response to poly(I:C), a mimic of viral dsRNA. Poly(I:C), acting via TLR3, induces p52-dependent transactivation of a reporter gene in a manner that requires the kinase activity of I?B kinase ? (IKK?) and the transactivating potential of RelA/p65. We identify a novel NF?B2 binding site in the promoter of the transcription factor Sp1 that is required for Sp1 gene transcription activated by poly(I:C). We show that Sp1 is required for IL-15 induction by both poly(I:C) and respiratory syncytial virus, a response that also requires NF?B2 and IKK?. Our study identifies NF?B2 as a target for IKK? in antiviral immunity and describes, for the first time, a role for NF?B2 in the regulation of gene expression in response to viral infection.

SUBMITTER: Doyle SL 

PROVIDER: S-EPMC3757171 | biostudies-literature | 2013 Aug

REPOSITORIES: biostudies-literature