Solá Castrillo, PalomaMereu, ElisabettaBonjoch, JúliaCasado Peláez, MartaPrats, NeusAguilera, MònicaReina, OscarBlanco, EnriqueEsteller, ManelCroce, Luciano DiHeyn, HolgerSolanas Fuster, GuiomarBenitah, Salvador A.2023-07-042023-07-042023-06-082662-8465https://hdl.handle.net/2445/200286Skin 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.© 2023. The Author(s).34 p.application/pdfengcc by (c) Solá Castrillo, Paloma et al, 2023http://creativecommons.org/licenses/by/3.0/es/ImmunitatPellEnvellimentImmunitySkinAginginfo:eu-repo/semantics/article2023-06-30info:eu-repo/semantics/openAccess659714837291218