Decision Letter: Role of Distinct Fibroblast Lineages and Immune Cells in Dermal Repair Following UV Radiation-Induced Tissue Damage

The study by Rognoni et al. found that different fibroblast populations in the skin respond differently to UV radiation and tissue remodeling. Papillary fibroblasts in the upper dermis are primarily responsible for tissue repair after acute UV radiation, but chronic UV damage is harder to repair due to a severe loss of these fibroblasts, a phenomenon also seen in aging skin. CD4 and CD8 T cells support UV-induced tissue repair by maintaining papillary fibroblasts. The study used gene expression profiles of different fibroblast subpopulations in undamaged neonatal and adult mouse skin, sun-exposed human eyelid skin, and microdissected human skin. After acute UVB exposure, all fibroblasts near the basement membrane in the upper dermis are depleted, but recover to baseline levels 14 days after exposure. Chronic UVB exposure, however, results in persistent depletion of upper fibroblasts. The study also found a significant loss of dermal fibroblasts in human skin 1 day post UV radiation, followed by a transient increase during the repair phase and a return to pre-exposure levels after two weeks. Both CD4+ and CD8+ T cells influence dermal fibroblast survival and proliferation, suggesting that UVB-induced inflammation affects dermal fibroblast survival, with increased fibroblast apoptosis and PGE-2 levels upon T cell depletion.