Fuente: PubMed "nature biotechnology" Front Immunol. 2026 Mar 16;17:1662245. doi: 10.3389/fimmu.2026.1662245. eCollection 2026.ABSTRACTVitiligo is an autoimmune disease characterized by the loss of skin pigmentation due to the loss of melanocytes. The pathogenesis of vitiligo is complex, involving multiple genetic factors, environmental triggers, oxidative stress, and autoimmunity against melanocytes. Stressed melanocytes release damage-associated molecular patterns, which trigger increased activation of antigen presenting cells, leading to maturation and activation of CD8+ T-cells that respond to auto-melanocyte-specific antigens. Once recruited to melanocytes, cytotoxic CD8+ and CD4+ T-cells produce cytokines, including primarily the type 1 cytokine IFN-γ, but also IL-2, IL-15, and type 2-related cytokines. Cytokines bind to fibroblasts, melanocytes, and keratinocytes to induce a positive feedback loop of immune cell recruitment to lesions, immune cell activation, and melanocyte apoptosis. The JAK/STAT pathway and TEC family kinase signaling play key roles in vitiligo pathogenesis through chemokine production, reduction of melanocyte adhesion, and immune cell activation and disease maintenance. This review summarizes recent key advances in understanding how these pathways impact vitiligo pathogenesis and details the emergence of new targeted therapies for the treatment of vitiligo.PMID:41918735 | PMC:PMC13033657 | DOI:10.3389/fimmu.2026.1662245