Monocytes in vitiliginous patients and normal volunteers showed sensitivity to alterations in methylation and revealed association between IL-10 and reactivity of autoimmune system. Methylation of deoxyribunucleic acid (DNA) conducted by DNA methyltransferases (DNMT1, -3a, -3b). However, patients with GV also linked to AIS3 locus (chromosome 8). In addition, CTLA4 had association secondarily with GV, and the autoimmune diseases. FOXP3 associated with X linked recessive multiple autoimmune disease syndrome. Of 33 tested loci, only (XBP1, TSLP, and FOXP3) were primarily concomitant with GV. Autoimmune susceptibility (AIS)-1, -2 (chromosome 7) and systemic lupus erythematosus vitiligo-related gene (SLEV1) (chromosome 17) both associated loci for GV and concomitant autoimmune diseases. Spritz et al (2004) revealed different loci or alleles for GV. Future research is needed to clarify the interaction of these factors for better understanding of vitiligo pathogenesis and subsequent successful treatment. It is a multifactorial disease involving the interplay of several factors. Many theories were elaborated to clarify vitiligo pathogenesis. We highlight the autoimmune hypothesis, followed by the reactive oxygen species model, zinc-α2-glycoprotein deficiency hypothesis, viral theory, intrinsic theory and biochemical, molecular and cellular alterations accounting for loss of functioning melanocytes in vitiligo. The discussion begun with the role of genetic predisposition followed by neural theory first proposed in the 1950s. This review article, we present the findings behind the most and updated theories behind this psychologically debilitating and disfiguring disease. Many studies across decades and all over the world have attempted to illustrate the pathogenesis behind it however, the pathogenesis of vitiligo remains elusive. Vitiligo is a common pigmentary disorder.
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