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Updated: Jul 27, 2025

Lymphocyte Isolation from Human Skin for Phenotypic Analysis and Ex Vivo Cell Culture
Published on: April 8, 2016
Targeting lymphoid-derived IL-17 signaling to delay skin aging
Paloma Solá1, Elisabetta Mereu2, Júlia Bonjoch1
1Institute for Research in Biomedicine, Barcelona Institute of Science and Technology, Barcelona, Spain.
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.
Insights
Aging skin exhibits chronic inflammation driven by increased IL-17 signaling. Blocking this pathway in mice delayed skin aging, suggesting a therapeutic target for age-related skin conditions.
Area of Science:
- Immunology
- Dermatology
- Aging Research
Background:
- Skin aging involves structural and functional decline, linked to local niche alterations and stem cell changes.
- Pro-inflammatory microenvironments significantly influence age-associated frailty and tissue aging.
- The specific inflammatory cues and their impact on skin aging remain largely unknown.
Purpose of the Study:
- To investigate the nature of age-associated inflammatory cues in mouse skin.
- To determine the role of IL-17 (interleukin-17) signaling in skin aging.
- To explore IL-17 blockade as a potential strategy to mitigate skin aging.
Main Methods:
- Single-cell RNA sequencing of the dermal compartment in aged mouse skin.
- In vivo blockade of IL-17 signaling during the aging process.
- Analysis of NF-κB signaling pathways in epidermal cells.
Main Results:
- Aged mouse skin shows a higher prevalence of IL-17-expressing T helper cells, γδ T cells, and innate lymphoid cells.
- In vivo IL-17 blockade reduced skin inflammation and delayed the onset of age-related skin traits.
- Aberrant IL-17 signaling activates NF-κB in epidermal cells, impairing homeostasis and promoting inflammation.
Conclusions:
- Aged skin is characterized by chronic inflammation, with IL-17 playing a key role.
- Targeting IL-17 signaling presents a promising therapeutic avenue for preventing age-associated skin ailments.
- Understanding IL-17's mechanism in epidermal cells offers insights into skin aging processes.
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