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IKKepsilon and TBK1 are essential components of the IRF3 signaling pathway.

Author information

Affiliations

  • 1. Division of Infectious Disease & Immunology, University of Massachusetts Medical School, Worcester, MA 01605, USA.
      Authors
    • Fitzgerald KA 1
    (1 author)

ORCIDs linked to this article

Nature Immunology, 01 May 2003, 4(5):491-496
https://doi.org/10.1038/ni921 PMID: 12692549 

A comment on this article appears in "Linking Toll-like receptors to IFN-alpha/beta expression." Nat Immunol. 2003 May;4(5):432-3.

Abstract 

The transcription factors interferon regulatory factor 3 (IRF3) and NF-kappaB are required for the expression of many genes involved in the innate immune response. Viral infection, or the binding of double-stranded RNA to Toll-like receptor 3, results in the coordinate activation of IRF3 and NF-kappaB. Activation of IRF3 requires signal-dependent phosphorylation, but little is known about the signaling pathway or kinases involved. Here we report that the noncanonical IkappaB kinase homologs, IkappaB kinase-epsilon (IKKepsilon) and TANK-binding kinase-1 (TBK1), which were previously implicated in NF-kappaB activation, are also essential components of the IRF3 signaling pathway. Thus, IKKepsilon and TBK1 have a pivotal role in coordinating the activation of IRF3 and NF-kappaB in the innate immune response.

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Read article at publisher's site: https://doi.org/10.1038/ni921

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Funding 

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NIAID NIH HHS (1)

NIGMS NIH HHS (1)