Review synthesizes Treg biology and NB-UVB, JAK inhibitors, IL-2 in vitiligo patients

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Frontiers in Medicine Published May 18, 2026 Medically reviewed May 18, 2026 DOI ↗ By Dr. Amelia Tan, PhD · Internal Medicine & Chronic Disease

Key Takeaway

Note that NB-UVB, JAK inhibitors, and low-dose IL-2 show promise in restoring immune balance in vitiligo.

This narrative review synthesizes current understanding of Treg biology and immunoregulatory functions in the context of vitiligo. The scope includes an analysis of Treg frequency, suppressive capacity, polarization, and specific subsets such as STAM+ Treg and exhausted memory Treg in both peripheral blood and lesional skin. The authors also discuss Treg-melanocyte interaction networks and related biomarkers.

The review reports that Treg frequency in peripheral blood is reduced in vitiligo patients. Additionally, Treg suppressive capacity is impaired, and Th1-like polarization is observed. In lesional skin, tissue-resident and antigen-specific Treg subsets are markedly decreased, and function is compromised by the proinflammatory microenvironment.

Regarding therapeutic interventions, the authors state that NB-UVB, JAK inhibitors, and low-dose IL-2 show promise in restoring immune balance. However, the review highlights that Treg abnormalities in vitiligo remain insufficiently integrated from a systemic perspective. Future single-cell transcriptomics and functionally defined Treg subsets may facilitate translation of Treg-based biomarkers and therapies into practice.

Study Details

Study typeSystematic review

EvidenceLevel 1

PublishedMay 2026

View Original Abstract ↓

IntroductionVitiligo 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.MethodsThis 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.ResultsIn 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.DiscussionThe 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.