In 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 IKKε and the transactivating potential of RelA/p65. We identify a novel NFκB2 binding site in the promoter of the transcription factor Sp1 which 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 Syncitial Virus, a response that also requires NFκB2 and IKKε. Our study identifies NFκB2 as a target for IKKε in anti -viral immunity and describes, for the first time, a role for NFκB2 in the regulation of gene expression in response to viral infection.