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Mellett, M.* ; Atzei, P.* ; Bergin, R.* ; Horgan, A.* ; Floß, T. ; Wurst, W. ; Callanan, J.J.* ; Moynagh, P.N.*

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

Nat. Commun. 6:6669 (2015)
Verlagsversion DOI PMC
Open Access Gold
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.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Nf-kappa-b; Domain-containing Adapter; Cutting Edge; Drosophila Toll; Activation; Pathway; Sef; Protein; Kinase; Family
Sprache englisch
Veröffentlichungsjahr 2015
HGF-Berichtsjahr 2015
ISSN (print) / ISBN 2041-1723
e-ISSN 2041-1723
Zeitschrift Nature Communications
Quellenangaben Band: 6, Heft: , Seiten: , Artikelnummer: 6669 Supplement: ,
Verlag Nature Publishing Group
Verlagsort London
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Developmental Genetics (IDG)
POF Topic(s) 30204 - Cell Programming and Repair
Forschungsfeld(er) Genetics and Epidemiology
PSP-Element(e) G-500500-001
PubMed ID 25808990
DOI 10.1038/ncomms7669
WOS ID WOS:000353042400003
Scopus ID 84925834283
Erfassungsdatum 2015-03-28
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