Study of Comparison of Serum CXCL10 in Vitiligenous Patients before and after NB-UVB

Abstract

itiligo is a disfiguring disease of the skin that affects ~0.5–2% of the population and results in prominent, disfiguring white spots that may become widespread (Agarwal et al., 2015). The exact etiology of vitiligo is unknown, but four main theories exist to explain it: the autoimmune hypothesis, the neural hypothesis, the self-destruct hypothesis, and the growth factor defect hypothesis. It is believed that Vitiligo pathogenesis incorporates both intrinsic defects within melanocytes that activate the cellular stress response, as well as autoimmune mechanisms that target these cells (Passeron and Ortonne, 2012; Spritz, 2012). And that a convergence theory, combining elements of different theories across a spectrum of expression is the most accurate etiology. Strong evidence in favor of the autoimmune hypothesis has been obtained. The autoimmune model proposes that melanocytes death occurs through inappropriate immune system destruction of pigment cells. Both cellular and humoral immunity co-operate in the destruction of melanocytes. The association of vitiligo with other known autoimmune disorders such as Addison’s disease, Hashimoto’s thyroiditis, pernicious anemia and alopecia areata also supports the autoimmune theory of disease (Kemp et al., 2001).