Please use this identifier to cite or link to this item:
http://hdl.handle.net/2445/200286
Title: | Targeting lymphoid-derived IL-17 signaling to delay skin aging |
Author: | Solá Castrillo, Paloma Mereu, Elisabetta Bonjoch, Júlia Casado Peláez, Marta Prats, Neus Aguilera, Mònica Reina, Oscar Blanco, Enrique Esteller, Manel Croce, Luciano Di Heyn, Holger Solanas Fuster, Guiomar Benitah, Salvador A. |
Keywords: | Immunitat Pell Envelliment Immunity Skin Aging |
Issue Date: | 8-Jun-2023 |
Publisher: | Springer Nature |
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.© 2023. The Author(s). |
Note: | Reproducció del document publicat a: https://doi.org/10.1038/s43587-023-00431-z |
It is part of: | Nature Aging, 2023, vol. 3, num. 6, p. 688-704 |
URI: | http://hdl.handle.net/2445/200286 |
Related resource: | https://doi.org/10.1038/s43587-023-00431-z |
ISSN: | 2662-8465 |
Appears in Collections: | Articles publicats en revistes (Institut de Recerca Biomèdica (IRB Barcelona)) |
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Solà_Aznar_NatAging_2023.pdf | 9.27 MB | Adobe PDF | View/Open |
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