Vitiligo is a complex disease, involving a combination of genetic and environmental factors, together with metabolic and immune alterations. Abnormalities leading to impaired melanocyte regeneration and/or proliferation suggest that defect(s) in melanocytes play an important role in this disease. However, it is becoming increasingly evident that inflammation and autoimmunity are also central players, in particular during the progressive phase of the disease. The critical role of the immune response during vitiligo pathogenesis has now largely been described and future emerging therapeutics are targeting the immune pathway. Indeed, most of the identified susceptibility genes (GWAS studies) are related to the immune system. Deregulation of the inflammasome and the JAK/STAT pathway has been highlighted, and Increasing evidence is pointing out the role of both innate (such as plasmacytoid dendritic cells, innate lymphoid cells, natural killer cells) and adaptive (in particular T cells) immune cells together with their related cytokines and chemokines during disease pathogenesis. In contrast, a defect in regulatory T cells number and/or function was reported. In addition, immunomodulating agents, such as JAK inhibitors, appear as promising therapeutic strategies for patients.
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