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A tissue injury sensing and repair pathway distinct from host pathogen defense.
Liu, Siqi; Hur, Yun Ha; Cai, Xin; Cong, Qian; Yang, Yihao; Xu, Chiwei; Bilate, Angelina M; Gonzales, Kevin Andrew Uy; Parigi, S Martina; Cowley, Christopher J; Hurwitz, Brian; Luo, Ji-Dung; Tseng, Tiffany; Gur-Cohen, Shiri; Sribour, Megan; Omelchenko, Tatiana; Levorse, John; Pasolli, Hilda Amalia; Thompson, Craig B; Mucida, Daniel; Fuchs, Elaine.
Affiliation
  • Liu S; Robin Chemers Neustein Laboratory of Mammalian Development and Cell Biology, Howard Hughes Medical Institute, The Rockefeller University, New York, NY 10065, USA.
  • Hur YH; Robin Chemers Neustein Laboratory of Mammalian Development and Cell Biology, Howard Hughes Medical Institute, The Rockefeller University, New York, NY 10065, USA.
  • Cai X; Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.
  • Cong Q; McDermott Center for Human Growth and Development, Department of Biophysics, and Harold C. Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
  • Yang Y; Robin Chemers Neustein Laboratory of Mammalian Development and Cell Biology, Howard Hughes Medical Institute, The Rockefeller University, New York, NY 10065, USA.
  • Xu C; Robin Chemers Neustein Laboratory of Mammalian Development and Cell Biology, Howard Hughes Medical Institute, The Rockefeller University, New York, NY 10065, USA.
  • Bilate AM; Laboratory of Mucosal Immunology, Howard Hughes Medical Institute, The Rockefeller University, New York, NY 10065, USA.
  • Gonzales KAU; Robin Chemers Neustein Laboratory of Mammalian Development and Cell Biology, Howard Hughes Medical Institute, The Rockefeller University, New York, NY 10065, USA.
  • Parigi SM; Robin Chemers Neustein Laboratory of Mammalian Development and Cell Biology, Howard Hughes Medical Institute, The Rockefeller University, New York, NY 10065, USA.
  • Cowley CJ; Robin Chemers Neustein Laboratory of Mammalian Development and Cell Biology, Howard Hughes Medical Institute, The Rockefeller University, New York, NY 10065, USA.
  • Hurwitz B; Robin Chemers Neustein Laboratory of Mammalian Development and Cell Biology, Howard Hughes Medical Institute, The Rockefeller University, New York, NY 10065, USA.
  • Luo JD; Bioinformatics Resource Center, The Rockefeller University, New York, NY 10065, USA.
  • Tseng T; Robin Chemers Neustein Laboratory of Mammalian Development and Cell Biology, Howard Hughes Medical Institute, The Rockefeller University, New York, NY 10065, USA.
  • Gur-Cohen S; Robin Chemers Neustein Laboratory of Mammalian Development and Cell Biology, Howard Hughes Medical Institute, The Rockefeller University, New York, NY 10065, USA.
  • Sribour M; Robin Chemers Neustein Laboratory of Mammalian Development and Cell Biology, Howard Hughes Medical Institute, The Rockefeller University, New York, NY 10065, USA.
  • Omelchenko T; Robin Chemers Neustein Laboratory of Mammalian Development and Cell Biology, Howard Hughes Medical Institute, The Rockefeller University, New York, NY 10065, USA.
  • Levorse J; Robin Chemers Neustein Laboratory of Mammalian Development and Cell Biology, Howard Hughes Medical Institute, The Rockefeller University, New York, NY 10065, USA.
  • Pasolli HA; Electron Microscopy Resource Center, The Rockefeller University, New York, NY 10065, USA.
  • Thompson CB; Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.
  • Mucida D; Laboratory of Mucosal Immunology, Howard Hughes Medical Institute, The Rockefeller University, New York, NY 10065, USA.
  • Fuchs E; Robin Chemers Neustein Laboratory of Mammalian Development and Cell Biology, Howard Hughes Medical Institute, The Rockefeller University, New York, NY 10065, USA. Electronic address: fuchslb@rockefeller.edu.
Cell ; 186(10): 2127-2143.e22, 2023 05 11.
Article in En | MEDLINE | ID: mdl-37098344
ABSTRACT
Pathogen infection and tissue injury are universal insults that disrupt homeostasis. Innate immunity senses microbial infections and induces cytokines/chemokines to activate resistance mechanisms. Here, we show that, in contrast to most pathogen-induced cytokines, interleukin-24 (IL-24) is predominately induced by barrier epithelial progenitors after tissue injury and is independent of microbiome or adaptive immunity. Moreover, Il24 ablation in mice impedes not only epidermal proliferation and re-epithelialization but also capillary and fibroblast regeneration within the dermal wound bed. Conversely, ectopic IL-24 induction in the homeostatic epidermis triggers global epithelial-mesenchymal tissue repair responses. Mechanistically, Il24 expression depends upon both epithelial IL24-receptor/STAT3 signaling and hypoxia-stabilized HIF1α, which converge following injury to trigger autocrine and paracrine signaling involving IL-24-mediated receptor signaling and metabolic regulation. Thus, parallel to innate immune sensing of pathogens to resolve infections, epithelial stem cells sense injury signals to orchestrate IL-24-mediated tissue repair.
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Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Wounds and Injuries / Cytokines Limits: Animals Language: En Journal: Cell Year: 2023 Type: Article Affiliation country: United States
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Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Wounds and Injuries / Cytokines Limits: Animals Language: En Journal: Cell Year: 2023 Type: Article Affiliation country: United States