Neurogenic dysregulation, oxidative stress, autoimmunity, and melanocytorrhagy in vitiligo: can they be interconnected?

Abstract

Several hypotheses have been proposed to explain vitiligo, including the neural theory, impaired redux status, autoimmunity, and more recently melanocytorrhagy arising from defective cell-cell adhesion. It is most likely that the loss of melanocytes in vitiligo arises through a combination of pathogenic mechanisms that act in concert. Here, we discuss the potential interconnection of several mechanisms that are likely to operate. These include the alteration of melanocyte-specific factors by reactive oxygen species to produce neo-antigens and the role of hypoxia and oxidative stress in antigen presentation and the auto-immune destruction of melanocytes.