{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T00:29:04Z","timestamp":1791419344559,"version":"4.3.3"},"reference-count":37,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2022,10,10]],"date-time":"2022-10-10T00:00:00Z","timestamp":1665360000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81971544"],"award-info":[{"award-number":["81971544"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81971545"],"award-info":[{"award-number":["81971545"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82172343"],"award-info":[{"award-number":["82172343"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Immunology"],"published-print":{"date-parts":[[2023,3]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Primary Sj\u00f6gren's syndrome (pSS) is a chronic systemic autoimmune disease characterized by B cell hyperactivation and hypergrammaglobulinemia. Currently, the role of metabolic pathways in the B cells of pSS patients is poorly defined. Here, we showed that upon cytosine phosphate\u2010guanine (CpG)\/sCD40L\/IL\u20104 stimulation, B cells proportionally increased glycolysis and oxygen consumption, and compared with B cells from healthy controls (HCs), B cells from pSS patients exhibited higher glycolysis capacity and maximal oxidative respiration (OXPHOS). We also found that glucose transporter 1 (GLUT1) expression in B cells from pSS patients was significantly higher than that in B cells from HCs. Treatment with 2\u2010deoxy\u2010\n                    <jats:sc>d<\/jats:sc>\n                    \u2010glucose (2\u2010DG) inhibited the activation of B cells in pSS patients. Both 2\u2010DG and Metformin inhibited the proliferation, formation of plasma\/plasmablasts and decreased the IgG and IgM levels in the supernatants of B cells from pSS patients. Furthermore, inhibition of mTORC1 by rapamycin had an effect similar to that of 2\u2010DG, suppressing B cell activation, proliferation and antibody production. Taken together, we demonstrated that B cells from pSS patients are more metabolically active than those from HCs and suggested that the mTORC1\u2010GLUT1 glycolysis pathways were the major drivers of B cell hyperactivation and autoantibody production in pSS patients.\n                  <\/jats:p>","DOI":"10.1111\/imm.13580","type":"journal-article","created":{"date-parts":[[2022,9,25]],"date-time":"2022-09-25T22:54:25Z","timestamp":1664146465000},"page":"432-443","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":19,"title":["mTORC1\u2010GLUT1\u2010mediated glucose metabolism drives hyperactivation of B cells in primary Sjogren's syndrome"],"prefix":"10.1111","volume":"168","author":[{"given":"Xuan","family":"Luo","sequence":"first","affiliation":[{"name":"Department of Rheumatology, Peking Union Medical College Hospital, Chinese Academy of Medical Science &amp; Peking Union Medical College, National Clinical Research Center for Dermatologic and Immunologic Diseases State Key Laboratory of Complex Severe and Rare Diseases  Beijing China"},{"name":"Department of Rheumatology, National Center for Children's Health, Beijing Children's Hospital Capital Medical University  Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xunyao","family":"Wu","sequence":"additional","affiliation":[{"name":"Clinical Biobank, Department of Medical Research Center, Peking Union Medical College Hospital Chinese Academy of Medical Sciences and Peking Union Medical College  Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anqi","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Rheumatology, Peking Union Medical College Hospital, Chinese Academy of Medical Science &amp; Peking Union Medical College, National Clinical Research Center for Dermatologic and Immunologic Diseases State Key Laboratory of Complex Severe and Rare Diseases  Beijing 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of Rheumatology, Peking Union Medical College Hospital, Chinese Academy of Medical Science &amp; Peking Union Medical College, National Clinical Research Center for Dermatologic and Immunologic Diseases State Key Laboratory of Complex Severe and Rare Diseases  Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lidan","family":"Zhao","sequence":"additional","affiliation":[{"name":"Department of Rheumatology, Peking Union Medical College Hospital, Chinese Academy of Medical Science &amp; Peking Union Medical College, National Clinical Research Center for Dermatologic and Immunologic Diseases State Key Laboratory of Complex Severe and Rare Diseases  Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Huaxia","family":"Yang","sequence":"additional","affiliation":[{"name":"Department of Rheumatology, Peking Union Medical College Hospital, Chinese Academy of Medical Science &amp; Peking Union Medical College, National Clinical Research 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