P204 Is Required for Canonical Lipopolysaccharide-induced TLR4 Signaling in Mice.

ABSTRACT: p204, a murine member of an interferon-inducible p200 family, was reported to recognize intracellular viral and bacterial DNAs, however, its role in the innate immunity in vivo remains unknown due to the lack of p204-deficient animal models. In this study we first generated the p204^-/- mice. Unexpectedly, p204 deficiency led to significant defect in extracellular LPS signaling in macrophages, as demonstrated by dramatic reductions of LPS-mediated IFN-β and pro-inflammatory cytokines. The serum levels of IFN-β and pro-inflammatory cytokines were also significantly reduced in p204^-/- mice following LPS challenge. In addition, p204^-/- mice were resistant to LPS-induced shock. LPS-activated NF-ĸB and IRF-3 pathways were all defective in p204-deficient macrophag

SUBMITTER: Yi YS 

PROVIDER: S-EPMC5925582 | biostudies-literature | 2018 Mar

REPOSITORIES: biostudies-literature