Search

Introduction: The pathogenesis of vitiligo is multifactorial; its diagnosis is mainly clinical and, in selected cases, is supported by histopathological studies that show the absence of melanocytes. The fundamental aspects of vitiligo are presented with emphasis on immunopathological events. Methodology: Narrative review. The PubMed® and Google Scholar search engines were used, with the following terms: "vitiligo", "vitiligo aetiology", "immunopathogenesis of vitiligo" and "vitiligo history". A total of 45 articles were selected, including Colombian literature. Results and discussion: Vitiligo is a disease as old as humanity. Until today, a clear causal phenomenon has not been established, but rather a set of events related to its origin and perpetuation. Thanks to decades of research, some genetic and environmental influences on melanocytes have been revealed, which lead to a greater susceptibility to oxidative damage and a decrease in their intercellular adhesion. In response to different noxa, innate and adaptive immunity are activated, leading to the destruction of the melanocyte mediated by cytotoxic CD8+ T cells. Participation of interferon-gamma (IFN-γ), the Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway, especially JAK-1 and JAK-2, and the CXCR3B chemokine receptor are highlighted. Conclusions: Multiple biological phenomena converge in the etiopathogenesis of vitiligo; the result is the activation of CD8+ T lymphocytes, responsible for the destruction of melanocytes. The understanding of immunopathogenic pathways opens the door to the use of target therapies, such as JAK inhibitors and CXCR3B inhibitors. [ABSTRACT FROM AUTHOR]