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      Role of Adaptor TRIF in the MyD88-Independent Toll-Like Receptor Signaling Pathway

      Science
      American Association for the Advancement of Science (AAAS)

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          Abstract

          Stimulation of Toll-like receptors (TLRs) triggers activation of a common MyD88-dependent signaling pathway as well as a MyD88-independent pathway that is unique to TLR3 and TLR4 signaling pathways leading to interferon (IFN)-beta production. Here we disrupted the gene encoding a Toll/IL-1 receptor (TIR) domain-containing adaptor, TRIF. TRIF-deficient mice were defective in both TLR3- and TLR4-mediated expression of IFN-beta and activation of IRF-3. Furthermore, inflammatory cytokine production in response to the TLR4 ligand, but not to other TLR ligands, was severely impaired in TRIF-deficient macrophages. Mice deficient in both MyD88 and TRIF showed complete loss of nuclear factor kappa B activation in response to TLR4 stimulation. These findings demonstrate that TRIF is essential for TLR3- and TLR4-mediated signaling pathways facilitating mammalian antiviral host defense.

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          Author and article information

          Journal
          Science
          Science
          American Association for the Advancement of Science (AAAS)
          0036-8075
          1095-9203
          August 01 2003
          August 01 2003
          : 301
          : 5633
          : 640-643
          Article
          10.1126/science.1087262
          12855817
          e19dcca0-a03f-476d-ae39-c0d9296c751a
          © 2003
          History

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