Orphan receptor IL-17RD regulates Toll-like receptor signalling via SEFIR/TIR interactions

Mark Mellett, Paola Atzei, Ronan Bergin, Alan Horgan, Thomas Floss, Wolfgang Wurst, John J. Callanan and Paul N. Moynagh ()
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Mark Mellett: Institute of Immunology, National University of Ireland Maynooth
Paola Atzei: Institute of Immunology, National University of Ireland Maynooth
Ronan Bergin: Institute of Immunology, National University of Ireland Maynooth
Alan Horgan: Institute of Immunology, National University of Ireland Maynooth
Thomas Floss: Helmholtz Zentrum München, Institute of Developmental Genetics
Wolfgang Wurst: Helmholtz Zentrum München, Institute of Developmental Genetics
John J. Callanan: UCD School of Veterinary Medicine & Conway Institute of Biomolecular & Biomedical Research, UCD
Paul N. Moynagh: Institute of Immunology, National University of Ireland Maynooth

Nature Communications, 2015, vol. 6, issue 1, 1-15

Abstract: Abstract Receptor families of the innate immune response engage in ‘cross-talk’ to tailor optimal immune responses against invading pathogens. However, these responses are subject to multiple levels of regulation to keep in check aberrant inflammatory signals. Here, we describe a role for the orphan receptor interleukin-17 receptor D (IL-17RD) in negatively regulating Toll-like receptor (TLR)-induced responses. Deficiency of IL-17RD expression in cells leads to enhanced pro-inflammatory signalling and gene expression in response to TLR stimulation, and Il17rd−/− mice are more susceptible to TLR-induced septic shock. We demonstrate that the intracellular Sef/IL-17R (SEFIR) domain of IL-17RD targets TIR adaptor proteins to inhibit TLR downstream signalling thus revealing a paradigm involving cross-regulation of members of the IL-17R and TLR families.

Date: 2015
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DOI: 10.1038/ncomms7669

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