title: IL-33-Dependent Group 2 Innate Lymphoid Cells Promote Cutaneous Wound Healing.
abstract: Breaches in the skin barrier initiate an inflammatory immune response that is critical for successful wound healing. Innate lymphoid cells (ILCs) are a recently identified population of immune cells that reside at epithelial barrier surfaces such as the skin, lung, and gut, and promote proinflammatory or epithelial repair functions after exposure to allergens, pathogens, or chemical irritants. However, the potential role of ILCs in regulating cutaneous wound healing remains undefined. Here, we demonstrate that cutaneous injury promotes an IL-33-dependent group 2 ILC (ILC2) response and that abrogation of this response impairs re-epithelialization and efficient wound closure. In addition, we provide evidence suggesting that an analogous ILC2 response is operational in acute wounds of human skin. Together, these results indicate that IL-33-responsive ILC2s are an important link between the cutaneous epithelium and the immune system, acting to promote the restoration of skin integrity after injury.
authors.affiliation: Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
authors.forename: Gregory D
authors.initials: GD
authors.lastname: Rak
authors.affiliation: Jill Roberts Institute for Research in IBD, Weill Cornell Medical College, Cornell University New York, New York, USA.
authors.forename: Lisa C
authors.initials: LC
authors.lastname: Osborne
authors.affiliation: Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
authors.forename: Mark C
authors.initials: MC
authors.lastname: Siracusa
authors.affiliation: Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
authors.forename: Brian S
authors.initials: BS
authors.lastname: Kim
authors.affiliation: Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
authors.forename: Kelvin
authors.initials: K
authors.lastname: Wang
authors.affiliation: Plastic & Reconstructive Surgery Research, Manchester Institute of Biotechnology, University of Manchester, Manchester, UK; Center for Dermatology, Institute of Inflammation and Repair, Faculty of Medical and Human Sciences, University of Manchester, Manchester Academic Health Science Centre, Manchester, UK.
authors.forename: Ardeshir
authors.initials: A
authors.lastname: Bayat
authors.affiliation: Jill Roberts Institute for Research in IBD, Weill Cornell Medical College, Cornell University New York, New York, USA. Electronic address: dartis@med.cornell.edu.
authors.forename: David
authors.initials: D
authors.lastname: Artis
authors.affiliation: Department of Clinical Studies-Philadelphia, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Electronic address: swvolk@vet.upenn.edu.
authors.forename: Susan W
authors.initials: SW
authors.lastname: Volk
mesh_terms: D000818:Animals; D001707:Biopsy, Needle; D004195:Disease Models, Animal; D006801:Humans; D007113:Immunity, Innate / Q000276:immunology / Q000502:physiology*; D007150:Immunohistochemistry; D000067596:Interleukin-33 / Q000276:immunology* / Q000378:metabolism; D008214:Lymphocytes / Q000166:cytology / Q000276:immunology; D051379:Mice; D008810:Mice, Inbred C57BL; D012867:Skin / Q000293:injuries* / Q000473:pathology; D014945:Wound Healing / Q000276:immunology* / Q000502:physiology; D014947:Wounds and Injuries / Q000276:immunology* / Q000473:pathology
chemical_list: D000067596:Interleukin-33