Frontiers in immunology · 2026
Regulatory T cells in vitiligo: a review of functional disequilibrium between peripheral blood and lesional tissue.
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Qiu Ye, He Yurong, Liu Fang
Аннотация
INTRODUCTION: Vitiligo is an autoimmune skin disorder driven by CD8+ T cell-mediated melanocyte destruction, in which breakdown of immune tolerance plays a pivotal role. Regulatory T cells (Tregs) are central to maintaining peripheral immune tolerance, but their abnormalities in vitiligo remain insufficiently integrated from a systemic perspective.
METHODS: This review synthesizes published evidence on Treg biology and immunoregulatory functions, focusing on comparative analyses between peripheral blood and lesional skin of vitiligo patients. We also examine Treg-melanocyte interaction networks, Treg-targeted therapies, and the potential of Treg-related biomarkers.
RESULTS: In peripheral blood, vitiligo patients exhibit reduced Treg frequency, impaired suppressive capacity, and Th1-like polarization, alongside dysfunctional subsets such as STAM (signal-transducing adaptor molecule)+ Treg and exhausted memory Treg. In lesional skin, tissue-resident and antigen-specific Treg subsets are markedly decreased, and the proinflammatory microenvironment further compromises their function. This systemic-to-local Treg dysregulation leads to insufficient suppression of autoreactive CD8+ T cells and persistent melanocyte destruction. Mechanistically, breakdown of the protective Treg-melanocyte network involves systemic Treg deficits, failure of local tolerance, melanocyte-intrinsic death programs, and disrupted homing/signaling. Therapeutically, NB-UVB, JAK inhibitors, and low-dose IL-2 show promise in restoring immune balance, and emerging Treg subsets may serve as biomarkers for treatment response.
DISCUSSION: The anatomical hierarchy of Treg dysregulation-from blood to skin-underscores that effective immunosuppression requires not only sufficient Treg numbers but also precise tissue localization and functional adaptation. Future single-cell transcriptomics and functionally defined Treg subsets may facilitate translation of Treg-based biomarkers and therapies into practice.
METHODS: This review synthesizes published evidence on Treg biology and immunoregulatory functions, focusing on comparative analyses between peripheral blood and lesional skin of vitiligo patients. We also examine Treg-melanocyte interaction networks, Treg-targeted therapies, and the potential of Treg-related biomarkers.
RESULTS: In peripheral blood, vitiligo patients exhibit reduced Treg frequency, impaired suppressive capacity, and Th1-like polarization, alongside dysfunctional subsets such as STAM (signal-transducing adaptor molecule)+ Treg and exhausted memory Treg. In lesional skin, tissue-resident and antigen-specific Treg subsets are markedly decreased, and the proinflammatory microenvironment further compromises their function. This systemic-to-local Treg dysregulation leads to insufficient suppression of autoreactive CD8+ T cells and persistent melanocyte destruction. Mechanistically, breakdown of the protective Treg-melanocyte network involves systemic Treg deficits, failure of local tolerance, melanocyte-intrinsic death programs, and disrupted homing/signaling. Therapeutically, NB-UVB, JAK inhibitors, and low-dose IL-2 show promise in restoring immune balance, and emerging Treg subsets may serve as biomarkers for treatment response.
DISCUSSION: The anatomical hierarchy of Treg dysregulation-from blood to skin-underscores that effective immunosuppression requires not only sufficient Treg numbers but also precise tissue localization and functional adaptation. Future single-cell transcriptomics and functionally defined Treg subsets may facilitate translation of Treg-based biomarkers and therapies into practice.