Nuclear factor κB2 p52 protein has a role in antiviral immunity through IκB kinase epsilon-dependent induction of Sp1 protein and interleukin 15.
Item Type:Journal Article
Citation:Doyle SL, Shirey KA, McGettrick AF, Kenny EF, Carpenter S, Caffrey BE, Gargan S, Quinn SR, Caamaño JH, Moynagh P, Vogel SN, O'Neill LA, Nuclear factor κB2 p52 protein has a role in antiviral immunity through IκB kinase epsilon-dependent induction of Sp1 protein and interleukin 15., J. Biol. Chem., 288, 35, 2013, 25066 - 25075
J. Biol. Chem.-2013-Doyle-25066-75.pdf (PDF) 2.239Mb
n this study we describe a previously unreported function for NFκB2, an NFκB family transcription factor, in antiviral immunity. NFκB2 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 IκB kinase ε (IKKε) and the transactivating potential of RelA/p65. We identify a novel NFκB2 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 NFκB2 and IKKε. Our study identifies NFκB2 as a target for IKKε in antiviral immunity and describes, for the first time, a role for NFκB2 in the regulation of gene expression in response to viral infection.
Type of material:Journal Article
Series/Report no:J. Biol. Chem.
Availability:Full text available