IL-17A-Exposed Senescent Fibroblasts Evade Apoptosis and Clearance

The skin is a tissue highly susceptible to damage from various stressors, including reactive oxygen species, UV radiation and chemical exposure. While damaged cells are often repaired, some sustain irreversible damage and become senescent. Although the body possesses mechanisms to remove these senescent cells, they accumulate with age for reasons that remain unclear. The close relationship between chronic inflammation and cellular senescence has recently become a major focus of research. Here, we sought to analyse the mechanisms driving age-related chronic inflammation and its impact on the accumulation of senescent cells. Our analysis of the cytokine IL-17A, a key factor in chronic inflammation, revealed that its levels increase in the skin with age. We also discovered that regulatory T cells (Treg cells), which typically act to suppress IL-17A, begin to secrete it as they age. Moreover, we found that IL-17A enhances the resistance of senescent cells to apoptosis. These results propose a model in which the age-related rise in the inflammatory factor IL-17A fosters an environment where senescent cells resist clearance, thereby promoting their accumulation.