摘要
In this study we describe a previously unreported function for NF kappa B2, an NF kappa B family transcription factor, in antiviral immunity. NF kappa 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 kappa B kinase epsilon (IKK epsilon) and the transactivating potential of RelA/p65. We identify a novel NF kappa 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 kappa B2 and IKK epsilon. Our study identifies NF kappa B2 as a target for IKK epsilon in antiviral immunity and describes, for the first time, a role for NF kappa B2 in the regulation of gene expression in response to viral infection.
- 出版日期2013-8-30