Epidermal Notch1 recruits RORγ+ group 3 innate lymphoid cells to orchestrate normal skin repair

Zhi Li, Tom Hodgkinson, Elizabeth J. Gothard, Soulmaz Boroumand, Rebecca Lamb, Ian Cummins, Priyanka Narang, Amy Sawtell, Jenny Coles, German Leonov, Andrea Reboldi, Christopher D. Buckley, Tom Cupedo, Christian Siebel, Ardeshir Bayat, Mark C. Coles () and Carrie A. Ambler ()
Additional contact information
Zhi Li: School of Biological and Biomedical Sciences, Biophysical Sciences Institute, Durham University
Tom Hodgkinson: Institute for Inflammation and Repair, University of Manchester
Elizabeth J. Gothard: Centre for Immunology and Infection
Soulmaz Boroumand: School of Biological and Biomedical Sciences, Biophysical Sciences Institute, Durham University
Rebecca Lamb: School of Biological and Biomedical Sciences, Biophysical Sciences Institute, Durham University
Ian Cummins: School of Biological and Biomedical Sciences, Biophysical Sciences Institute, Durham University
Priyanka Narang: Centre for Immunology and Infection
Amy Sawtell: Centre for Immunology and Infection
Jenny Coles: Centre for Immunology and Infection
German Leonov: Centre for Immunology and Infection
Andrea Reboldi: University of California
Christopher D. Buckley: MRC Centre for Immune Regulation, University of Birmingham
Tom Cupedo: Erasmus University Medical Center
Christian Siebel: Genentech Inc
Ardeshir Bayat: Institute for Inflammation and Repair, University of Manchester
Mark C. Coles: Centre for Immunology and Infection
Carrie A. Ambler: School of Biological and Biomedical Sciences, Biophysical Sciences Institute, Durham University

Nature Communications, 2016, vol. 7, issue 1, 1-14

Abstract: Abstract Notch has a well-defined role in controlling cell fate decisions in the embryo and the adult epidermis and immune systems, yet emerging evidence suggests Notch also directs non-cell-autonomous signalling in adult tissues. Here, we show that Notch1 works as a damage response signal. Epidermal Notch induces recruitment of immune cell subsets including RORγ+ ILC3s into wounded dermis; RORγ+ ILC3s are potent sources of IL17F in wounds and control immunological and epidermal cell responses. Mice deficient for RORγ+ ILC3s heal wounds poorly resulting from delayed epidermal proliferation and macrophage recruitment in a CCL3-dependent process. Notch1 upregulates TNFα and the ILC3 recruitment chemokines CCL20 and CXCL13. TNFα, as a Notch1 effector, directs ILC3 localization and rates of wound healing. Altogether these findings suggest that Notch is a key stress/injury signal in skin epithelium driving innate immune cell recruitment and normal skin tissue repair.

Date: 2016
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms11394

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DOI: 10.1038/ncomms11394

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