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

Zhi Li, Christopher Buckley, 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

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49 Citations (Scopus)
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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


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