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- W2040706148 abstract "Interferon regulatory factors (IRFs) are critical components of virus-induced immune activation and type I interferon regulation. IRF3 and IRF7 are activated in response to a variety of viruses or after engagement of Toll-like receptor (TLR) 3 and TLR4 by double-stranded RNA and lipopolysaccharide, respectively. The activation of IRF5, is much more restricted. Here we show that in contrast to IRF3 and IRF7, IRF5 is not a target of the TLR3 signaling pathway but is activated by TLR7 or TLR8 signaling. We also demonstrate that MyD88, interleukin 1 receptor-associated kinase 1, and tumor necrosis factor receptor-associated factor 6 are required for the activation of IRF5 and IRF7 in the TLR7 signaling pathway. Moreover, ectopic expression of IRF5 enabled type I interferon production in response to TLR7 signaling, whereas knockdown of IRF5 by small interfering RNA reduced type I interferon induction in response to the TLR7 ligand, R-848. IRF5 and IRF7, therefore, emerge from these studies as critical mediators of TLR7 signaling." @default.
- W2040706148 created "2016-06-24" @default.
- W2040706148 creator A5009349672 @default.
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- W2040706148 date "2005-04-01" @default.
- W2040706148 modified "2023-10-16" @default.
- W2040706148 title "The Interferon Regulatory Factor, IRF5, Is a Central Mediator of Toll-like Receptor 7 Signaling" @default.
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- W2040706148 doi "https://doi.org/10.1074/jbc.m412584200" @default.
- W2040706148 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/15695821" @default.
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