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Immunohistochemical study of perforin and apoptosis stimulation fragment ligand (FasL)in active vitiligo

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Abstract

Several studies demonstrated a major pathological role of melanocyte-specific cytotoxic CD8+ T cells in the pathogenesis of vitiligo. It has been suggested that apoptosis, rather than necrosis, is the mechanism of melanocyte depletion in vitiligo. The aim of this study was to evaluate the expression and distribution of perforin and apoptosis stimulation fragment ligand (FasL) in the epidermis and dermis of the perilesional and non-lesional skin of vitiligo patients in comparison to controls, to assess their possible role in mediating apoptosis in vitiligo. Twenty patients with active non-segmental vitiligo and 20 healthy controls were enrolled in the study. Skin biopsies were taken from perilesional and non-lesional skin of patients with vitiligo, as well as covered skin of controls. Immunostaining for perforin and FasL was performed and the quantitative analysis for the expression of perforin and FasL was carried out in the epidermis and dermis of biopsied specimens. Epidermal perforin, dermal perforin, epidermal FasL, dermal FasL were significantly higher in perilesional as well as non-lesional skin than controls. There was a statistically significant positive correlation between epidermal and dermal perforin in perilesional skin. There was a statistically significant positive correlation between epidermal and dermal perforin, as well as epidermal and dermal FasL in non-lesional skin. In conclusion, the significant expression of perforin and FasL in the epidermis and dermis of both perilesional and non-lesional skin of active vitiligo patients suggests the role of cytotoxic granules and apoptotic cell death pathways in the pathogenesis of active vitiligo.

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Correspondence to Sara Bahaa Mahmoud.

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Hassan, A.S., Kohil, M.M., Sayed, S.S.E. et al. Immunohistochemical study of perforin and apoptosis stimulation fragment ligand (FasL)in active vitiligo. Arch Dermatol Res 313, 453–460 (2021). https://doi.org/10.1007/s00403-020-02117-7

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