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

Research output: Contribution to journalArticlepeer-review


  • Tom Hodgkinson
  • Elizabeth J Gothard
  • Soulmaz Boroumand
  • Rebecca Lamb
  • Ian Cummins
  • Priyanka Narang
  • Amy Sawtell
  • Jenny Coles
  • German Leonov
  • Andrea Reboldi
  • Tom Cupedo
  • Christian Siebel
  • Ardeshir Bayat
  • Mark C Coles
  • Carrie A Ambler


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.


Original languageEnglish
Article number11394
JournalNature Communications
Publication statusPublished - 21 Apr 2016