Abstract
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.
Highlights
Vitiligo is an acquired, chronic skin disorder characterized by epidermal melanocyte loss and the clinical appearance of patchy depigmentation on the skin
Together with IFN-γ, IFN-α enhances the secretion of CXCL9 and CXCL10 from keratinocytes to amplify the infiltration of CXCR3-expressing immune cells in lesional skin [54, 55]
These studies have provided evidence for the crosstalk between oxidative stress and autoimmune response orchestrated by chemotactic signals interferon-CXCL9/10-CXCR3 axis
Summary
Chronic skin disorder characterized by epidermal melanocyte loss and the clinical appearance of patchy depigmentation on the skin. Early analysis of chemokines in vitiligo indicated that the expression of chemokines, such as CXCL9 and CXCL10, could be reliable biomarkers for disease activity and prognosis, emerging studies have shed light on the interaction between the increased ROS levels and levels of several chemokines, such as CXCL16 and CXCL10, to act as key effectors in the initiation and progression of vitiligo [10]. These ROS-induced chemokines further mediate the migration of immune cells, especially T cells, in the lesion of vitiligo patients [10, 11]. We focus on the sources and expressions of these chemokines in the context of vitiligo and reveal the functional roles and underlying mechanisms involved in the interaction between oxidative stress and autoimmunity in the pathogenesis and progression of vitiligo, which might further provide insight into potential treatment approaches for vitiligo patients
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