{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T06:32:58Z","timestamp":1791268378027,"version":"4.1.0"},"reference-count":97,"publisher":"F1000 Research Ltd","license":[{"start":{"date-parts":[[2016,9,6]],"date-time":"2016-09-06T00:00:00Z","timestamp":1473120000000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["f1000research.com"],"crossmark-restriction":false},"short-container-title":["F1000Res"],"abstract":"<ns4:p>Vitiligo, an acquired depigmentation disorder, manifests as white macules on the skin and can cause significant psychological stress and stigmatization. Recent advances have shed light on key components that drive disease onset and progression as well as therapeutic approaches. Vitiligo can be triggered by stress to the melanin pigment-producing cells of the skin, the melanocytes. The triggers, which range from sunburn to mechanical trauma and chemical exposures, ultimately cause an autoimmune response that targets melanocytes, driving progressive skin depigmentation. The most significant progress in our understanding of disease etiology has been made on three fronts: (1) identifying cellular responses to stress, including antioxidant pathways and the unfolded protein response (UPR), as key players in disease onset, (2) characterizing immune responses that target melanocytes and drive disease progression, and (3) identifying major susceptibility genes. The current model for vitiligo pathogenesis postulates that oxidative stress causes cellular disruptions, including interruption of protein maturation in the endoplasmic reticulum (ER), leading to the activation of the UPR and expression of UPR-regulated chemokines such as interleukin 6 (IL-6) and IL-8. These chemokines recruit immune components to the skin, causing melanocytes to be targeted for destruction. Oxidative stress can further increase melanocyte targeting by promoting antigen presentation. Two key components of the autoimmune response that promote disease progression are the interferon (IFN)-\u03b3\/CXCL10 axis and IL-17-mediated responses. Several genome-wide association studies support a role for these pathways, with the antioxidant gene<ns4:italic>NRF2<\/ns4:italic>, UPR gene<ns4:italic>XBP1<\/ns4:italic>, and numerous immune-related genes including class I and class II major histocompatibility genes associated with a risk for developing vitiligo. Novel approaches to promote repigmentation in vitiligo are being investigated and may yield effective, long-lasting therapies.<\/ns4:p>","DOI":"10.12688\/f1000research.8976.1","type":"journal-article","created":{"date-parts":[[2016,9,6]],"date-time":"2016-09-06T09:35:22Z","timestamp":1473154522000},"page":"2234","update-policy":"https:\/\/doi.org\/10.12688\/f1000research.crossmark-policy","source":"Crossref","is-referenced-by-count":85,"title":["Recent advances in understanding vitiligo"],"prefix":"10.12688","volume":"5","author":[{"given":"Prashiela","family":"Manga","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nada","family":"Elbuluk","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Seth 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Harris, Department of Medicine, Division of Dermatology, University of Massachusetts Medical School, Worcester, MA, USA, 06 Sep 2016, version 1, indexed","URL":"https:\/\/f1000research.com\/articles\/5-2234\/v1#referee-response-16121","order":2,"name":"referee-response-16121","label":"Referee Report","group":{"name":"article-reports","label":"Article Reports"}},{"value":"Research reported in this publication was supported in part by the National Institute of Arthritis and Musculoskeletal and Skin Diseases, part of the National Institutes of Health (NIH), under Award AR41880 (Seth J. Orlow). The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH. 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