生物
自分泌信号
先天免疫系统
旁分泌信号
伤口愈合
趋化因子
信号转导
祖细胞
炎症
细胞生物学
再生(生物学)
获得性免疫系统
免疫系统
干细胞
受体
免疫学
生物化学
作者
Siqi Liu,Yun Ha Hur,Xin Cai,Qian Cong,Yihao Yang,Chiwei Xu,Angelina M. Bilate,Kevin Andrew Uy Gonzales,Sara Martina Parigi,Christopher Cowley,Brian Hurwitz,Ji‐Dung Luo,Tiffany W. Tseng,Shiri Gur-Cohen,Megan Sribour,Tatiana Omelchenko,John Levorse,H. Amalia Pasolli,Craig B. Thompson,Daniel Mucida,Elaine Fuchs
出处
期刊:Cell
[Elsevier]
日期:2023-05-01
卷期号:186 (10): 2127-2143.e22
被引量:14
标识
DOI:10.1016/j.cell.2023.03.031
摘要
Summary
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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