TY - JOUR
T1 - IL-33-Dependent Group 2 Innate Lymphoid Cells Promote Cutaneous Wound Healing
AU - Rak, Gregory D.
AU - Osborne, Lisa C.
AU - Siracusa, Mark C.
AU - Kim, Brian S.
AU - Wang, Kelvin
AU - Bayat, Ardeshir
AU - Artis, David
AU - Volk, Susan W.
N1 - Funding Information:
We thank Matthew Hepworth, Jonathan Brestoff, Becky Brisson, and Yanjian Wang for technical assistance as well as members of the Artis lab for review of this manuscript. We also thank Tianying Jiang and the Cancer Histology Core for their assistance. This research was supported by the National Institutes of Health (AI061570, AI074878, AI106697, AI095466, AI095608, AI102942, and AI097333 to DA; K08AR053945 to SWV; T32-AR007465, and KL2-RR024132 to BSK; and F32-AI085828 to MCS); the Crohn’s and Colitis Foundation of America (to DA); the Burroughs Wellcome Fund Investigator in Pathogenesis of Infectious Disease Award (to DA). These studies were supported by NIH/NIDDK P30 Center for Molecular Studies in Digestive and Liver Diseases (P30-DK050306), its pilot grant program and scientific core facilities (Molecular Pathology and Imaging, Molecular Biology, Cell Culture and Mouse).
Publisher Copyright:
© 2015 The Authors
PY - 2016
Y1 - 2016
N2 - 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.
AB - 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.
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U2 - 10.1038/JID.2015.406
DO - 10.1038/JID.2015.406
M3 - Article
C2 - 26802241
AN - SCOPUS:84973633011
SN - 0022-202X
VL - 136
SP - 487
EP - 496
JO - Journal of Investigative Dermatology
JF - Journal of Investigative Dermatology
IS - 2
ER -