| First Author | Li Z | Year | 2016 |
| Journal | Nat Commun | Volume | 7 |
| Pages | 11394 | PubMed ID | 27099134 |
| Mgi Jnum | J:236882 | Mgi Id | MGI:5810038 |
| Doi | 10.1038/ncomms11394 | Citation | Li Z, et al. (2016) Epidermal Notch1 recruits RORgamma(+) group 3 innate lymphoid cells to orchestrate normal skin repair. Nat Commun 7:11394 |
| abstractText | 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 RORgamma(+) ILC3s into wounded dermis; RORgamma(+) ILC3s are potent sources of IL17F in wounds and control immunological and epidermal cell responses. Mice deficient for RORgamma(+) ILC3s heal wounds poorly resulting from delayed epidermal proliferation and macrophage recruitment in a CCL3-dependent process. Notch1 upregulates TNFalpha and the ILC3 recruitment chemokines CCL20 and CXCL13. TNFalpha, 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. |
