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Trends Mol Med. 2007 Nov;13(11):460-9. Epub 2007 Oct 29.

Signaling to NF-kappaB by Toll-like receptors.

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1
Department of Host Defense and Exploratory Research for Advanced Technology, Japan Science and Technology Agency, Research Institute for Microbial Diseases, Osaka University, 3-1 Yamada-oka, Suita, Osaka 565-0871, Japan.

Abstract

Innate immunity is the first line of defense against invading pathogens. A family of Toll-like receptors (TLRs) acts as primary sensors that detect a wide variety of microbial components and elicit innate immune responses. All TLR signaling pathways culminate in activation of the transcription factor nuclear factor-kappaB (NF-kappaB), which controls the expression of an array of inflammatory cytokine genes. NF-kappaB activation requires the phosphorylation and degradation of inhibitory kappaB (IkappaB) proteins, which is triggered by two kinases, IkappaB kinase alpha (IKKalpha) and IKKbeta. In addition, several TLRs activate alternative pathways involving the IKK-related kinases TBK1 [TRAF family member-associated NF-kappaB activator (TANK) binding kinase-1] and IKKi, which elicit antiviral innate immune responses. Here, we review recent progress in our understanding of the role of NF-kappaB in TLR signaling pathways and discuss potential implications for molecular medicine.

PMID:
18029230
DOI:
10.1016/j.molmed.2007.09.002
[Indexed for MEDLINE]
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