{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,28]],"date-time":"2026-10-28T22:57:59Z","timestamp":1793228279322,"version":"4.5.0"},"reference-count":28,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,5,18]],"date-time":"2026-05-18T00:00:00Z","timestamp":1779062400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:sec>\n                    <jats:title>Introduction<\/jats:title>\n                    <jats:p>\n                      Vitiligo is an autoimmune skin disorder driven by CD8\n                      <jats:sup>+<\/jats:sup>\n                      T cell\u2212mediated 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.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>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\u2212melanocyte interaction networks, Treg\u2212targeted therapies, and the potential of Treg\u2212related biomarkers.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      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)\n                      <jats:sup>+<\/jats:sup>\n                      Treg and exhausted memory Treg. In lesional skin, tissue\u2212resident and antigen\u2212specific Treg subsets are markedly decreased, and the proinflammatory microenvironment further compromises their function. This systemic\u2212to\u2212local Treg dysregulation leads to insufficient suppression of autoreactive CD8\n                      <jats:sup>+<\/jats:sup>\n                      T cells and persistent melanocyte destruction. Mechanistically, breakdown of the protective Treg\u2212melanocyte network involves systemic Treg deficits, failure of local tolerance, melanocyte\u2212intrinsic death programs, and disrupted homing\/signaling. Therapeutically, NB\u2212UVB, JAK inhibitors, and low\u2212dose IL\u22122 show promise in restoring immune balance, and emerging Treg subsets may serve as biomarkers for treatment response.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Discussion<\/jats:title>\n                    <jats:p>The anatomical hierarchy of Treg dysregulation\u2014from blood to skin\u2014underscores that effective immunosuppression requires not only sufficient Treg numbers but also precise tissue localization and functional adaptation. Future single\u2212cell transcriptomics and functionally defined Treg subsets may facilitate translation of Treg\u2212based biomarkers and therapies into practice.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fimmu.2026.1844106","type":"journal-article","created":{"date-parts":[[2026,5,18]],"date-time":"2026-05-18T05:41:58Z","timestamp":1779082918000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":3,"title":["Regulatory T cells in vitiligo: a review of functional disequilibrium between peripheral blood and lesional tissue"],"prefix":"10.3389","volume":"17","author":[{"given":"Ye","family":"Qiu","sequence":"first","affiliation":[{"name":"Department of Dermatology, Beijing Chaoyang Hospital, Capital Medical University","place":["Beijing, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yurong","family":"He","sequence":"additional","affiliation":[{"name":"Department of Dermatology, Beijing Chaoyang Hospital, Capital Medical University","place":["Beijing, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fang","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Dermatology, Beijing Chaoyang Hospital, Capital Medical University","place":["Beijing, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,5,18]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"74","DOI":"10.1016\/S0140-6736(14)60763-7","article-title":"Vitiligo","volume":"386","author":"Ezzedine","year":"2015","journal-title":"Lancet"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.3390\/ijms25137171","article-title":"Regulatory T cell dysfunction in autoimmune diseases","volume":"25","author":"Honing","year":"2024","journal-title":"Int J Mol Sci"},{"key":"B3","doi-asserted-by":"publisher","first-page":"1586","DOI":"10.1016\/j.immuni.2024.05.023","article-title":"The 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