Interferon-α induction through Toll-like receptors involves a direct interaction of IRF7 with MyD88 and TRAF6

By Taro Kawai, Shintaro Sato, K. Ishii, C. Coban, H. Hemmi, Masahiro Yamamoto, K. Terai, M. Matsuda, J. Inoue, Satoshi Uematsu and 2 more. Nature Immunology, 2004

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Toll-like receptor function and signaling. (2006, background): “IRF-7 colocalizes with MyD88 in endosomal vesicles, whereas IRF-3 does not.(49,50) IRF-7 can directly associate with MyD88 or TRAF6, forming a large molecular complex that leads to type I IFN production.”
Identification and Characterization of MAVS, a Mitochondrial Antiviral Signaling Protein that Activates NF-κB and IRF3 (2005, positive): “TLR3 contains an intracellular Toll-interleukin receptor (TIR) domain that signals to NF-κB and IRF3 via the adaptor protein TRIF (Akira and Takeda, 2004), whereas the TIR domain of TLR7 and TLR8 binds to another adaptor MyD88, which associates with and activates IRF7 to induce interferon-α (Kawai e”
Molecular determinants of crosstalk between nuclear receptors and toll-like receptors. (2005, background): “As IRF7 is involved in TLR9-MyD88-dependent gene activation (Kawai et al., 2004), these results imply that the mechanism of GR-mediated repression operates through both IRF3 and IRF7.”
Ubiquitin signalling in the NF-κB pathway (2005, background): “Indeed, TRAF6 ubiquitination has recently been found to be important for activation of the transcription factor interferon regulatory factor 7 (IRF7; ref”
Innate Immunity to Virus Infection (2009, background): “TLR7 and TLR9 recruit MyD88, which forms a complex with IRAK-1, IRAK-4, and IRF-7 in this cell type (79, 80).”