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Psoriasis is a common, chronic inflammatory skin disease characterized by cutaneous inflammation and epidermal hyperproliferation.The pathogenesis of psoriasis involves a complex interplay among the immune system, genetic susceptibility, and various environmental triggers.Although the immunopathogenesis of psoriasis has been extensively investigated, primarily emphasizing the IL-23/IL-17 pathogenic axis and the roles of Th17 cells, keratinocytes, and dendritic cells, the contributions of non-immune cells such as fibroblasts and endothelial cells remain to be fully elucidated.Dermal fibroblasts are integral to the maintenance of skin structural integrity, modulation of immune responses, and tissue repair following injury.Emerging evidence suggests that dysregulated fibroblast function contributes significantly to the initiation and perpetuation of chronic inflammatory processes observed in psoriasis.This review aims to provide a comprehensive overview of the current understanding regarding the role of fibroblasts in the pathogenesis of psoriasis, based on a review of the current literatures.
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Yun et al. (2025) studied this question.
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