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Epidermal Notch1 recruits RORγ(+) group 3 innate lymphoid cells to orchestrate normal skin repair.
Li, Zhi; Hodgkinson, Tom; Gothard, Elizabeth J; Boroumand, Soulmaz; Lamb, Rebecca; Cummins, Ian; Narang, Priyanka; Sawtell, Amy; Coles, Jenny; Leonov, German; Reboldi, Andrea; Buckley, Christopher D; Cupedo, Tom; Siebel, Christian; Bayat, Ardeshir; Coles, Mark C; Ambler, Carrie A.
Afiliación
  • Li Z; School of Biological and Biomedical Sciences, Biophysical Sciences Institute, Durham University, Durham DH1 3LE, UK.
  • Hodgkinson T; Centre for Immunology and Infection, Department of Biology and Hull York Medical School, York YO10 5DD, UK.
  • Gothard EJ; Institute for Inflammation and Repair, University of Manchester, Manchester M1 7DN, UK.
  • Boroumand S; Centre for Immunology and Infection, Department of Biology and Hull York Medical School, York YO10 5DD, UK.
  • Lamb R; School of Biological and Biomedical Sciences, Biophysical Sciences Institute, Durham University, Durham DH1 3LE, UK.
  • Cummins I; School of Biological and Biomedical Sciences, Biophysical Sciences Institute, Durham University, Durham DH1 3LE, UK.
  • Narang P; School of Biological and Biomedical Sciences, Biophysical Sciences Institute, Durham University, Durham DH1 3LE, UK.
  • Sawtell A; Centre for Immunology and Infection, Department of Biology and Hull York Medical School, York YO10 5DD, UK.
  • Coles J; Centre for Immunology and Infection, Department of Biology and Hull York Medical School, York YO10 5DD, UK.
  • Leonov G; Centre for Immunology and Infection, Department of Biology and Hull York Medical School, York YO10 5DD, UK.
  • Reboldi A; Centre for Immunology and Infection, Department of Biology and Hull York Medical School, York YO10 5DD, UK.
  • Buckley CD; Department of Microbiology and Immunology, University of California, San Francisco, California 94143, USA.
  • Cupedo T; MRC Centre for Immune Regulation, University of Birmingham, Birmingham B15 2TT, UK.
  • Siebel C; Department of Hematology, Erasmus University Medical Center, Rotterdam 3015CN, Netherlands.
  • Bayat A; Department of Molecular Biology, Division of Research, Genentech Inc, South San Francisco, California 94080, USA.
  • Coles MC; Institute for Inflammation and Repair, University of Manchester, Manchester M1 7DN, UK.
  • Ambler CA; Centre for Immunology and Infection, Department of Biology and Hull York Medical School, York YO10 5DD, UK.
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.
Asunto(s)

Texto completo: 1 Banco de datos: MEDLINE Asunto principal: Heridas Penetrantes / Subgrupos Linfocitarios / Epidermis / Receptor Notch1 / Miembro 3 del Grupo F de la Subfamilia 1 de Receptores Nucleares / Inmunidad Innata Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Año: 2016 Tipo del documento: Article

Texto completo: 1 Banco de datos: MEDLINE Asunto principal: Heridas Penetrantes / Subgrupos Linfocitarios / Epidermis / Receptor Notch1 / Miembro 3 del Grupo F de la Subfamilia 1 de Receptores Nucleares / Inmunidad Innata Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Año: 2016 Tipo del documento: Article