الفهرس 
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Abstract
Vitiligo is an autoimmune skin disease producing cells of the skin, are targeted for destruction by autoreactive CD8+ T cells. As a result, patients develop patchy white spots on their skin. Vitiligo affects roughly 1% of the population (Riding and Harris, 2019).
Melanocyte-specific, cytotoxic CD8+ T cells have been strongly implicated in the destruction of melanocytes in multiple studies. CD8+ T cell infiltration of the epidermis and dermis has been demonstrated histologically, in addition, higher numbers of cytotoxic CD8+ T cells in the blood were found in patients with vitiligo compared to healthy controls (Benzekri and Gauthier, 2017). Cytokines are key mediators of melanocyte loss in vitiligo and participate at every step of the pathogenesis of this disease (Migayron et al., 2020). Previous studies have demonstrated increased expression of inflammatory cytokines in skin and circulation among vitiligo patients (Rajendiran et al., 2020).
The mechanism of melanocyte loss in vitiligo is possibly related to keratinocyte-derived cytokines that stimulate melanocytes such as bFGF and SCF, or to those that inhibit melanocytes such as IL-6 andTNF-α. SCF is an essential factor for melanocyte survival (Tarlé et al., 2014).
Vitiligo affects approximately 1% of the