Literature DB >> 23892079

IRF3 and ERK MAP-kinases control nitric oxide production from macrophages in response to poly-I:C.

Tyler C Moore1, Thomas M Petro.   

Abstract

Understanding nitric oxide (NO) in innate anti-viral immunity and immune-mediated pathology is hampered by incomplete details of its transcriptional and signaling factors. We found in macrophages that IRF3, ERK MAP-kinases, and PKR are essential to NO production in response to RNA-virus mimic, poly I:C, a TLR3 agonist. ERK's role in NO induction may be through phosphorylation of serine-171 of IRF3 and expression of NO-inducing cytokines, IL-6 and IFN-β. However, these cytokines induced less NO in IRF3 knockout or knockdown macrophages. These findings show that ERK and IRF3 coordinate induction of NO by macrophages in response to stimulation of TLR3.
Copyright © 2013 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

Entities:  

Keywords:  BL/6; C57BL/6 mice; ERK; ERK MAP-kinase; IRF3; IRF3 deficient mice; IRF3KO; Interferon response factor-3; Interleukin-6; LPS; Macrophages; NF-κB; NO; Nitric oxide; ODN; PI3K; PKR; Poly I:C; TIR; TIR domain-containing adaptor-inducing IFN-β; TLR; TRIF; extracellular signal related kinase; interferon response factor 3; lipopolysaccharide; nitric oxide; nuclear factor κ-B; oligodeoxynucleotide; phosphoinositide-3-kinase; protein kinase R; toll like receptor; toll/IL-1 receptor

Mesh：

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Year:  2013        PMID： 23892079      PMCID： PMC3777643          DOI： 10.1016/j.febslet.2013.07.025

Source DB:  PubMed          Journal:  FEBS Lett        ISSN： 0014-5793            Impact factor:   4.124


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