Abstract
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).
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
