Cutting Edge: A Novel Toll/IL-1 Receptor Domain-Containing Adapter That Preferentially Activates the IFN-β Promoter in the Toll-Like Receptor Signaling1

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Interferons and viruses: an interplay between induction, signalling, antiviral responses and virus countermeasures. (2008, background): “Although TLR4 utilizes MyD88 to activate NF-kB, it uses the same adaptor as TLR3 (namely TRIF) to activate IRF-3 (Yamamoto et al., 2002; Oshiumi et al., 2003).”
Pathogen Recognition and Inflammatory Signaling in Innate Immune Defenses (2009, neutral): “Thus, molecular signaling mechanisms within the TRIF-dependent pathway illustrate how selective binding of different molecules, i.e., either TRAF3 or TRAF6, results in recruitment and downstream activation of TBK1-IRF versus TAK1-IKK-NF- B, respectively (Fig.”
Toll-like receptors and innate immunity (2006, background): “However, cells doubly deficient in TRAF6 and MyD88 still partially activated NF-κB in response to LPS, suggesting that TRIF activates NF-κB through both TRAF6-dependent and TRAF6-independent pathways in TLR4 signaling [65, 66].”
The adaptor protein MITA links virus-sensing receptors to IRF3 transcription factor activation. (2008, background): “Engagement of TLR3 by dsRNA triggers TRIF (an adaptor of the TLR pathway)-mediated signaling pathways, thereby leading to IRF3 and NF-kB activation (Han et al., 2004; Oshiumi et al., 2003; Yamamoto et al., 2003; Yamamoto et al., 2002).”