{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T01:38:51Z","timestamp":1790213931903,"version":"4.1.0"},"reference-count":36,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2025,9,14]],"date-time":"2025-09-14T00:00:00Z","timestamp":1757808000000},"content-version":"vor","delay-in-days":13,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["MedComm"],"published-print":{"date-parts":[[2025,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Systemic lupus erythematosus (SLE) is an autoimmune disease of unknown origin. Recent evidence has linked butyrophilin 3A1 (BTN3A1) to immune dysregulation. This study was to elucidate the relationship of BTN3A1 in SLE. Expression of BTN3A1 in plasma and peripheral blood mononuclear cells from SLE patients and healthy controls explored the association between BTN3A1 and SLE. We found that BTN3A1 mRNA, plasma levels, and expression in CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cells were significantly elevated in SLE patients. In BTN3A1 gene knock\u2010in (BTN3A1\n                    <jats:sup>KI<\/jats:sup>\n                    ) mice, inflammation and lupus\u2010like manifestations occurred, including increased proportions of Th1, Th2, and Th17 cells, decreased Treg cells, elevated levels of inflammatory cytokines and anti\u2010dsDNA antibodies, renal injury, and suppressed IL\u201038 serum levels. Intraperitoneal injection of IL\u201038 in pristane\u2010treated BTN3A1\n                    <jats:sup>KI<\/jats:sup>\n                    mice notably alleviated these pathological changes. Mechanistic investigations revealed that CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cells and the ferroptosis pathway were closely associated with the effects mediated by the BTN3A1\u2010IL\u201038 axis. In vitro experiments showed that IL\u201038 stimulation reduced proliferation, apoptosis, and decreased the expression of ferroptosis\u2010related proteins, Fe\n                    <jats:sup>2<\/jats:sup>\n                    \u207a, glutathione, and malondialdehyde in CD4\n                    <jats:sup>+<\/jats:sup>\n                    BTN3A1\n                    <jats:sup>+\/+<\/jats:sup>\n                    T and BTN3A1\n                    <jats:sup>+\/+<\/jats:sup>\n                    Jurkat T cells. Overall, BTN3A1 plays a crucial role in SLE pathogenesis by regulating CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cell function.\n                  <\/jats:p>","DOI":"10.1002\/mco2.70356","type":"journal-article","created":{"date-parts":[[2025,9,15]],"date-time":"2025-09-15T04:18:37Z","timestamp":1757909917000},"source":"Crossref","is-referenced-by-count":2,"title":["Butyrophilin 3A1 Contributes to Inflammation and Induces a Lupus\u2010Like Disease by Inhibiting the IL\u201038\u2010Ferroptosis Axis"],"prefix":"10.1002","volume":"6","author":[{"given":"Wang\u2010Dong","family":"Xu","sequence":"first","affiliation":[{"name":"Department of Evidence\u2010Based Medicine, School of Public Health Southwest Medical University  Luzhou Sichuan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Da\u2010Cheng","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Evidence\u2010Based Medicine, School of Public Health Southwest Medical University  Luzhou Sichuan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yang\u2010Yang","family":"Tang","sequence":"additional","affiliation":[{"name":"Department of Evidence\u2010Based Medicine, School of Public Health Southwest Medical University  Luzhou Sichuan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qi","family":"Huang","sequence":"additional","affiliation":[{"name":"Vanke School of Public Health Tsinghua University  Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lu","family":"Fu","sequence":"additional","affiliation":[{"name":"Laboratory Animal Center Southwest Medical University  Luzhou Sichuan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"You\u2010Yue","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Evidence\u2010Based Medicine, School of Public Health Southwest Medical University  Luzhou Sichuan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lu\u2010Qi","family":"Yang","sequence":"additional","affiliation":[{"name":"Department of Evidence\u2010Based Medicine, School of Public Health Southwest Medical University  Luzhou Sichuan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Si\u2010Yu","family":"Feng","sequence":"additional","affiliation":[{"name":"Department of Evidence\u2010Based Medicine, School of Public Health Southwest Medical University  Luzhou Sichuan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lin\u2010Chong","family":"Su","sequence":"additional","affiliation":[{"name":"Hubei Provincial Key Laboratory of Occurrence and Intervention of Rheumatic Diseases Affiliated Minda Hospital of Hubei Minzu University  Enshi Hubei China"},{"name":"Department of Rheumatology and Immunology Affiliated Minda Hospital of Hubei Minzu University  Enshi Hubei China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3860-8383","authenticated-orcid":false,"given":"An\u2010Fang","family":"Huang","sequence":"additional","affiliation":[{"name":"Department of Rheumatology and Immunology the Affiliated Hospital Southwest Medical University  Luzhou Sichuan China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2025,9,14]]},"reference":[{"key":"e_1_2_10_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.jaut.2022.102870"},{"key":"e_1_2_10_3_1","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2017.34"},{"key":"e_1_2_10_4_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.molmed.2017.05.006"},{"key":"e_1_2_10_5_1","doi-asserted-by":"publisher","DOI":"10.3389\/fimmu.2024.1520570"},{"key":"e_1_2_10_6_1","doi-asserted-by":"publisher","DOI":"10.3390\/ijms232113424"},{"key":"e_1_2_10_7_1","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0038541"},{"key":"e_1_2_10_8_1","doi-asserted-by":"publisher","DOI":"10.18632\/oncotarget.165"},{"key":"e_1_2_10_9_1","first-page":"648","article-title":"The V\u03b39V\u03b42 T Cell Antigen Receptor and Butyrophilin\u20103 A1: Models of Interaction, the Possibility of Co\u2010Evolution, and the Case of Dendritic Epidermal T 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