Vitiligo is a chronic autoimmune disease, caused due to selective destruction of melanocytes. It is characterized by depigmentation of skin. The mechanisms that underlie this phenomenon has not been clearly understood. Therefore, the aim of this review was to collate all the emerging information regarding the involvement of molecular components in vitiligo pathogenesis. Initial surveys suggested that certain chemicals were responsible for causing this skin disease. Recent genetic studies like twin studies show that vitiligo arises due to hereditary factors. Certain predisposing risk variants have been identified through can-didate gene studies and Genome-Wide Association Studies (GWAS). Skin biopsies and peripheral blood of vitiligo patients have revealed the presence of melanocyte targeting autoantibodies, increased T-cells and high levels of inflammatory cytokines, indicating that both humoral and cellular immunities play a major role in selective destruction of melanocytes. In addition to this, studies have shown the association of vitiligo with other autoimmune diseases, implicating that complications of other autoimmune diseases could lead to the development of vitiligo. Further research is required to understand the immune pathway of vitiligo and its commonness with other autoimmune disorders. This would help in tackling the disease therapeutically. Keywords: Vitiligo, Genetics, Autoimmunity, Human Leukocyte Antigen, Cytokines
Background: Vitiligo is an autoimmune disorder involving inflammatory damage to melanocytes. STAT3 genetic variant (rs744166 T > C) increases inflammatory signaling via JAK/STAT pathway. Aim: The purpose of this study was to check whether this translates into an association between vitiligo and STAT3 gene variant (rs744166 T > C). Materials and Methods: This is a case-control study. A total of 56 vitiligo patients and 90 healthy, age and gender-matched volunteers were recruited for the study. The STAT3 gene variant (rs744166 T > C) was genotyped using the restriction fragment length polymorphism method. Results: The frequency of the minor allele ‘C’ was higher in vitiligo patients (72.3%) than in healthy volunteers (57.8%). The difference between the two groups was statistically significant (P = 0.006; OR = 1.9 with 95% CI). The genotypic variant showed the highest association with vitiligo in the dominant model (P = 0.001). Conclusion: This study shows that the STAT3 gene variant (rs744166 T > C) is associated with vitiligo. This observation underlines the importance of the JAK/STAT signaling pathway in vitiligo pathogenesis.
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