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

Author

Listed:
  • 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
    Centre for Infection and Immunity, School of Medicine, Dentistry and Biomedical Sciences, Queen’s University Belfast)

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.

Suggested Citation

  • Mark Mellett & Paola Atzei & Ronan Bergin & Alan Horgan & Thomas Floss & Wolfgang Wurst & John J. Callanan & Paul N. Moynagh, 2015. "Orphan receptor IL-17RD regulates Toll-like receptor signalling via SEFIR/TIR interactions," Nature Communications, Nature, vol. 6(1), pages 1-15, May.
    • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms7669
    DOI: 10.1038/ncomms7669
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