Neurogenic dysregulation, oxidative stress, autoimmunity, and melanocytorrhagy in vitiligo: can they be interconnected?
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.
Namazi
M R
MR
Department of Dermatology, Shiraz University of Medical sciences, Shiraz, Iran. namazi_mr@yahoo.com
D000818:Animals; D001327:Autoimmune Diseases / Q000378:metabolism / Q000473:pathology*; D002384:Catalysis; D002448:Cell Adhesion; D004817:Epidermis / Q000378:metabolism; D005786:Gene Expression Regulation; D006801:Humans; D008544:Melanocytes / Q000166:cytology* / Q000378:metabolism; D008954:Models, Biological; D008962:Models, Theoretical; D009474:Neurons / Q000378:metabolism; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D017382:Reactive Oxygen Species; D014820:Vitiligo / Q000175:diagnosis* / Q000276:immunology* / Q000473:pathology
D017382:Reactive Oxygen Species