The outermost layer of the skin, the epidermis, is a stratified epithelium that forms an impermeable protection for the organism. The skin contains a multilayered epidermis interspersed with hair follicles and sebaceous glands. 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.Īging is caused by cellular damage accumulation due to ineffective metabolism, circadian clock rewiring and increased systemic inflammation, leading to dysfunction and eventual organismal collapse when challenged 1, 2, 3, 4, 5, 6. Mechanistically, aberrant IL-17 signals through NF-κB in epidermal cells to impair homeostatic functions while promoting an inflammatory state. Importantly, in vivo blockade of IL-17 signaling during aging reduces the proinflammatory state of the skin, delaying the appearance of age-related traits. 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. The nature of these age-associated inflammatory cues, or how they affect tissue aging, is unknown. This probably depends on synergy between alterations in the local niche and stem cell-intrinsic changes, underscored by proinflammatory microenvironments that drive pleotropic changes. Skin aging is characterized by structural and functional changes that contribute to age-associated frailty.
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