Abstract
Melanocytes in patients with vitiligo possess intrinsic abnormalities that contribute to its pathogenesis. In this issue, Regazzetti, et al. report that CXCL10 expression reflects subtle inflammation in normal-appearing skin but not in stable depigmented lesions, supporting the hypothesis that melanocytes themselves initiate autoimmune inflammation prior to clinically evident disease. In addition, they find that oxidative stress in melanocytes impairs WNT signaling and that targeting this pathway induces melanoblast differentiation. Thus, activating the WNT pathway may serve as an adjunctive strategy to support repigmentation in patients with vitiligo.
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