Orphan receptor IL-17RD tunes IL-17A signalling and is required for neutrophilia

Mark Mellett, Paola Atzei, Alan Horgan, Emily Hams, Thomas Floss, Wolfgang Wurst, Padraic G. Fallon 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
Alan Horgan: Institute of Immunology, National University of Ireland Maynooth
Emily Hams: Institute of Molecular Medicine, School of Medicine, Trinity College Dublin
Thomas Floss: Helmholtz Zentrum München, Institute of Developmental Genetics
Wolfgang Wurst: Helmholtz Zentrum München, Institute of Developmental Genetics
Padraic G. Fallon: Institute of Molecular Medicine, School of Medicine, Trinity College Dublin
Paul N. Moynagh: Institute of Immunology, National University of Ireland Maynooth

Nature Communications, 2012, vol. 3, issue 1, 1-10

Abstract: Abstract Interleukin-17A, the prototypical member of the interleukin-17 cytokine family, coordinates local tissue inflammation by recruiting neutrophils to sites of infection. Dysregulation of interleukin-17 signalling has been linked to the pathogenesis of inflammatory diseases and autoimmunity. The interleukin-17 receptor family members (A–E) have a broad range of functional effects in immune signalling yet no known role has been described for the remaining orphan receptor, interleukin-17 receptor D, in regulating interleukin-17A-induced signalling pathways. Here we demonstrate that interleukin-17 receptor D can differentially regulate the various pathways employed by interleukin-17A. Neutrophil recruitment, in response to in vivo administration of interleukin-17A, is abolished in interleukin-17 receptor D-deficient mice, correlating with reduced interleukin-17A-induced activation of p38 mitogen-activated protein kinase and expression of the neutrophil chemokine MIP-2. In contrast, interleukin-17 receptor D deficiency results in enhanced interleukin-17A-induced activation of nuclear factor-kappa B and interleukin-6 and keratinocyte chemoattractant expression. Interleukin-17 receptor D disrupts the interaction of Act1 and TRAF6 causing differential regulation of nuclear factor-kappa B and p38 mitogen-activated protein kinase signalling pathways.

Date: 2012
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DOI: 10.1038/ncomms2127

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