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

Author

Listed:
  • Zhi Li

    (School of Biological and Biomedical Sciences, Biophysical Sciences Institute, Durham University
    Centre for Immunology and Infection)

  • 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)

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.

Suggested Citation

  • 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 , 2016. "Epidermal Notch1 recruits RORγ+ group 3 innate lymphoid cells to orchestrate normal skin repair," Nature Communications, Nature, vol. 7(1), pages 1-14, September.
    • Handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms11394
    DOI: 10.1038/ncomms11394
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