促炎细胞因子
炎症
表型
生物
细胞生物学
免疫学
先天性淋巴细胞
舱室(船)
干细胞
免疫系统
先天免疫系统
遗传学
基因
海洋学
地质学
作者
Paloma Solá,Elisabetta Mereu,Júlia Bonjoch,Marta Casado-Peláez,Neus Prats,Mónica Aguilera,Oscar Reina,Enrique Blanco,Manel Esteller,Luciano Di Croce,Holger Heyn,Guiomar Solanas,Salvador Aznar Benitah
出处
期刊:Nature Aging
日期:2023-06-08
卷期号:3 (6): 688-704
被引量:16
标识
DOI:10.1038/s43587-023-00431-z
摘要
Abstract Skin aging is characterized by structural and functional changes that contribute to age-associated frailty. This probably depends on synergy between alterations in the local niche and stem cell-intrinsic changes, underscored by proinflammatory microenvironments that drive pleotropic changes. The nature of these age-associated inflammatory cues, or how they affect tissue aging, is unknown. Based on single-cell RNA sequencing of the dermal compartment of mouse skin, we show a skew towards an IL-17-expressing phenotype of T helper cells, γδ T cells and innate lymphoid cells in aged skin. Importantly, in vivo blockade of IL-17 signaling during aging reduces the proinflammatory state of the skin, delaying the appearance of age-related traits. Mechanistically, aberrant IL-17 signals through NF-κB in epidermal cells to impair homeostatic functions while promoting an inflammatory state. Our results indicate that aged skin shows signs of chronic inflammation and that increased IL-17 signaling could be targeted to prevent age-associated skin ailments.
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