Abstract
ABSTRACT
Vitiligo is an acquired depigmentation disorder characterized by the loss of epidermal melanocytes and can markedly impair patients' quality of life. Because of its dual effects on immunosuppression and repigmentation, UVB phototherapy has become a first‐line treatment for vitiligo. It is particularly valuable in inducing repigmentation of skin lesions. Since epidermal melanocytes are markedly reduced or even absent in vitiligo lesions, migration of melanocyte stem cells (McSCs) from the hair follicle bulge to the interfollicular epidermis is considered a critical step in UVB‐induced repigmentation, as it enables the replenishment of epidermal melanocytes. Therefore, this review summarizes the molecular mechanisms by which UVB induces McSC migration. Current evidence suggests that UVB primarily regulates McSC migration, proliferation, and differentiation indirectly by remodeling the McSC niche. In this process, keratinocytes, inflammatory cells, and other niche‐associated cells release multiple paracrine mediators, including SCF, EDN1, bFGF, PGE2, and WNT. These factors coordinately regulate the physiological activities of McSCs. In addition, we propose that changes in the expression of melanocyte surface receptors may be an important limiting factor governing the migratory response of McSCs. This review also discusses the molecular markers of McSCs and the physiological changes that accompany their migration. Based on current evidence, we further hypothesize that some melanocytes migrating to the epidermis may retain the ability to dedifferentiate and return to the hair follicle. This process may represent an important mechanism by which UVB‐induced McSC migration does not deplete the McSC reservoir.