Epidermal Notch1 recruits RORγ(+) group 3 innate lymphoid cells to orchestrate normal skin repair.
Nat Commun
; 7: 11394, 2016 Apr 21.
Article
en En
| MEDLINE
| ID: mdl-27099134
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.
Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
Heridas Penetrantes
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Subgrupos Linfocitarios
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Epidermis
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Receptor Notch1
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Miembro 3 del Grupo F de la Subfamilia 1 de Receptores Nucleares
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Inmunidad Innata
Tipo de estudio:
Prognostic_studies
Límite:
Animals
Idioma:
En
Año:
2016
Tipo del documento:
Article