Increased Activation of Innate Immunity and Pro-Apoptotic CXCR3B in Normal-Appearing Skin on the Lesional Site of Patients with Segmental Vitiligo

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The mechanisms involved in the pathogenesis of segmental vitiligo (SV) are poorly understood. Owing to its characteristic asymmetric unilateral distribution of depigmentation, proposed hypotheses include melanocytes and/or keratinocytes carrying mosaic mutation and being intrinsically abnormal and/or more susceptible to stress. Moreover, a subclinical inflammatory response is now well-demonstrated also in segmental forms of vitiligo (Speeckaert et al., 2020) and the involvement of CD8+ melanocyte-specific T-cell‒mediated immunity as is observed in generalized vitiligo (van Geel et al., 2010).