Skin aging is a natural process that leads to changes in the skin's structural and functional properties. As we age, the skin becomes less resilient, leading to slower wound healing and a higher risk of infections. These changes contribute to age-associated frailty and can have a significant impact on an individual's quality of life.
A new study published at Nature Aging sheds light on the precise nature and origin of the age-associated inflammatory cues that drive skin aging. Using deep single-cell RNA-sequencing, we analyzed the entire dermal compartment of aged skin and found a previously unreported skew towards an IL-17–expressing phenotype of Th cells, γδ T cells, and innate lymphoid cells.
This is significant because aberrant IL-17 signaling is common to many autoimmune and chronic inflammatory diseases such as rheumatoid arthritis and psoriasis. Our study suggests that the aged skin shows chronic and persistent signs of inflammation, which could be targeted as a strategy to prevent age-associated skin ailments in the elderly.
Furthermore, we found that in vivo blockade of IL-17–triggered signaling during the aging process reduces the pro-inflammatory state by affecting immune and non-immune skin cells of both dermis and epidermis. Strikingly, IL-17 neutralization significantly delays the appearance of age-related traits such as decreased epidermal thickness, increased cornified layer thickness, and ameliorated hair follicle stem cell activation and hair shaft regeneration.
Our findings suggest that age-associated increased IL-17 signaling could be targeted as a strategy to prevent age-associated skin ailments in the elderly. This study provides a comprehensive understanding of the age-associated changes in all skin cell types, paving the way for new approaches to prevent and treat skin aging.