EXPLORING THE ROLE OF IMMUNOMETABOLISM AND MICROBIOME IN VITILIGO: OPPORTUNITIES FOR NEW THERAPEUTICS

Vitiligo, a chronic autoimmune depigmentation disorder affecting 0.5-2% globally, manifests through melanocyte destruction driven by immunometabolic dysregulation, oxidative stress, and gut microbiota dysbiosis. This review elucidates metabolic reprogramming in immune cells—monocytes shifting to glycolysis, M1 macrophages favoring PPP, and CD8+ T cells/TRMs relying on FAO—alongside gut-skin axis disruptions marked by reduced SCFAs, altered bile acids, and tryptophan metabolites that exacerbate IFN-γ/CXCL10-mediated inflammation. Emerging therapies targeting JAK-STAT, Nrf2-ARE, IL-15/CD122, and microbiome modulation offer promising avenues for restoring immune-metabolic homeostasis and achieving durable repigmentatio. Vitiligo emerges as a systemic immunometabolic disorder in which oxidative stress, immune dysregulation, and gut microbiota–derived metabolites converge to drive melanocyte destruction and defective repigmentation.