LAUSR

Vitiligo is a common chronic autoimmune skin disorder featured with depigmented patches and underlying destruction of melanocytes in the lesional skin. Multiple factors and mechanisms have been proposed for the etiopathogenesis of vitiligo, among which oxidative stress has been widely accepted as a key factor in initiating melanocyte loss. The altered redox status caused by oxidative stress, including the overproduction of reactive oxygen species (ROS) and the decreased activity of the antioxidant system in the skin, surrenders the resistance of melanocytes to exogenous or endogenous stimuli and eventually impairs the normal defense mechanism, leading to the absence of melanocytes. Considering the important role of innate and adaptive immunity in vitiligo, there is mounting evidence revealing an association between oxidative stress and autoimmunity. Since the significant changes of chemokines have been documented in vitiligo in many recent studies, it has been suggested that ROS-mediated chemotactic signals are not only the biomarkers of disease progression and prognosis but also are involved in the pathogenesis of vitiligo by facilitating the innate and adaptive immune cells, especially melanocyte-specific T cells, trafficking to the lesional areas of vitiligo. In this review, we discuss the interaction between oxidative stress and autoimmune response orchestrated by chemokines, including CXCL16-CXCR6 axis, CXCL9/CXCL10-CXCR3 axis, and other altered chemokines in vitiligo, and we also try to provide insight into potential therapeutic options through targeting these pathways.