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Please use this identifier to cite or link to this item: https://hdl.handle.net/2445/200286
Targeting lymphoid-derived IL-17 signaling to delay skin aging
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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.© 2023. The Author(s).
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SOLÁ CASTRILLO, Paloma, et al. Targeting lymphoid-derived IL-17 signaling to delay skin aging. Nature Aging. 2023. Vol. 3, num. 6, pags. 688-704. ISSN 2662-8465. [consulted: 8 of June of 2026]. Available at: https://hdl.handle.net/2445/200286