{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,3]],"date-time":"2026-06-03T18:28:35Z","timestamp":1780511315383,"version":"3.54.1"},"reference-count":29,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2025,12,22]],"date-time":"2025-12-22T00:00:00Z","timestamp":1766361600000},"content-version":"vor","delay-in-days":355,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2025,1,1]],"date-time":"2025-01-01T00:00:00Z","timestamp":1735689600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Mediators of Inflammation"],"published-print":{"date-parts":[[2025,1]]},"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Vitiligo is a common depigmentary disorder characterized by progressive melanocyte (MEL) loss. While T\u2010cell activation is central to its pathogenesis, the role of macrophages remains poorly understood. This study characterizes macrophage heterogeneity and function in vitiligo using single\u2010cell transcriptomic analysis and experimental validation.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We analyzed single\u2010cell RNA sequencing (scRNA\u2010seq) data from healthy and vitiligo\u2010affected skin to identify macrophage subpopulations. Computational analyses included cell subpopulation clustering, pseudotime trajectory inference, cell\u2013cell communication, and high\u2010dimensional weighted gene coexpression network analysis (hdWGCNA). In vivo and in vitro experiments examined the effects of STAT1 suppression on the macrophage inflammatory phenotype and antigen presentation capacity.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>scRNA\u2010seq analysis identified macrophages and T cell subsets enriched in vitiligo. Macrophage subclustering identified five subpopulations, with inflammatory antigen\u2010presenting macrophages (Mac\u2010InflamAP) significantly enriched in vitiligo lesions and M1\u2010polarized. Pseudotime analysis revealed Mac\u2010InflamAP as a terminal differentiation state. Cell\u2013cell communication analysis showed Mac\u2010InflamAP exerts TNF\u2010mediated inhibitory effects on MELs while enhancing T\u2010cell antigen presentation, thereby promoting MEL loss. hdWGCNA identified STAT1 as a key regulator highly expressed in Mac\u2010InflamAP. In vivo, STAT1 inhibition by fludarabine ameliorated vitiligo progression by suppressing T cell activation and macrophage M1\u2010polarization. In vitro experiments confirmed STAT1 suppression reduced macrophage M1 polarization, inflammatory phenotype, and antigen presentation capabilities.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>This study reveals an uncharacterized inflammatory macrophage subpopulation crucial to vitiligo pathogenesis through dual mechanisms: direct MEL inhibition and enhanced T\u2010cell activation. The identification of STAT1 as a key regulatory molecule provides a novel therapeutic target for vitiligo. These findings advance our understanding of immune\u2010mediated mechanisms in vitiligo.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1155\/mi\/8878698","type":"journal-article","created":{"date-parts":[[2025,12,23]],"date-time":"2025-12-23T07:48:57Z","timestamp":1766476137000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Single\u2010Cell Transcriptomic Analysis Reveals an Inflammatory Antigen\u2010Presenting Macrophages Subtype Drive Vitiligo Pathogenesis Through STAT1\u2010Mediated Dual 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