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

The study investigated the role of fibroblast lineages and immune cells in dermal repair following UV radiation-induced damage. It was found that acute and chronic UVR exposure led to a selective loss of fibroblasts in the upper dermis. Papillary fibroblast proliferation and migration were key in repairing acute UVR damage, while chronic exposure resulted in permanent fibroblast loss. The study highlighted that UVR activated Wnt-signalling, but epidermal β-catenin stabilisation did not aid in dermis repair. Acute UVR increased neutrophil and T cell infiltration, with CD4 and CD8 cell depletion exacerbating fibroblast loss and DNA damage. Topical COX-2 inhibition was effective in preventing fibroblast depletion and neutrophil infiltration. The findings suggested that fibroblast loss was primarily due to a deregulated inflammatory response, with T cells playing a supportive role in fibroblast survival under UVR stress.