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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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The interferon regulatory factor, IRF5, is a central mediator of toll-like receptor 7 signaling.

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.[1]

References

  1. The interferon regulatory factor, IRF5, is a central mediator of toll-like receptor 7 signaling. Schoenemeyer, A., Barnes, B.J., Mancl, M.E., Latz, E., Goutagny, N., Pitha, P.M., Fitzgerald, K.A., Golenbock, D.T. J. Biol. Chem. (2005) [Pubmed]
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