PATHOGENESIS OF NONSEGMENTAL VITILIGO: THE ROLE OF THE IFN-Γ–CXCL10 AXIS, TISSUE-RESIDENT MEMORY T CELLS, AND OXIDATIVE STRESS

Resume. The article provides an analytical overview of modern perspectives on the pathogenesis of non-segmental vitiligo, focusing on the role of the IFN-γ-CXCL10 axis, tissue-resident T-cell memory, and oxidative stress. Non-segmental vitiligo is considered a multifactorial autoimmune skin disease based on the selective damage and loss of epidermal melanocytes. The aim of the study was to study the modern pathogenetic mechanisms of non-segmental vitiligo development and to evaluate the significance of the IFN-γ-CXCL10 signaling pathway, TRM cells, and oxidative stress in the progression of depigmentation and disease recurrence. The materials of the study were scientific publications presented in the databases PubMed, Scopus, Web of Science, ScienceDirect, SpringerLink and Google Scholar. Analytical, comparative, descriptive, and generalizing methods were used. It has been established that oxidative stress is one of the early factors in melanocyte damage, contributing to the accumulation of active forms of oxygen, disruption of mitochondrial function, decrease in cell viability, and release of autoantigen. Activation of the IFN-γ-CXCL10-axis ensures the migration of CXCR3-positive CD8+ T-lymphocytes into the skin and maintains a self-sustaining inflammatory cycle that leads to the progressive destruction of melanocytes. Tissue-resident memory T-cells remain in previously affected areas of the skin and play a crucial role in the chronic course and recurrence of the disease. The obtained data indicate that oxidative stress, the IFN-γ-CXCL10 signaling pathway, and TRM cells are interconnected links in a single pathogenetic process and can be considered promising diagnostic, prognostic, and therapeutic targets for non-segmental vitiligo. Keywords: non-segmental vitiligo, IFN-γ, CXCL10, CXCR3, tissue resident memory T cells, TRM cells, oxidative stress, melanocytes, autoimmunity, depigmentation.

Перевод пока недоступен