Current Understanding of the Etiology of Vitiligo

Abstract

This article discusses the current understanding of the etiology of vitiligo. Vitiligo is defined as the loss of pigment-producing cells, melanocytes, from the epidermis of the skin. The onset of vitiligo is believed to require the following three components: (1) a complex of vitiligo susceptibility genes that influence the autoimmune response; (2) genetically abnormal melanocytes; and (3) one or more environmental or physiological factors that induce oxidative stress and activate the genetic program for melanocyte destruction. Melanocytes from vitiligo patients appear to be unable to combat oxidative stress, and so sustain damage. This significant damage could trigger apoptosis in the cells and create an environment rich with cellular fragments that could become autoimmune targets and activate an immune response against melanocytes. Alternatively, oxidatively stressed vitiligo melanocytes could produce cytokines and/or self-antigens to recruit a genetically reactive autoimmune response. Possible therapeutic targets include genes that regulate the immune response, or proteins like iHSP70 that are secreted by the vitiligo cell in response to oxidative stress. Vitiligo is a disease that impacts 1 % of the population and has social, psychological, and sexual ramifications for patients.