{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,30]],"date-time":"2026-10-30T00:02:34Z","timestamp":1793318554189,"version":"4.5.0"},"reference-count":75,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"824","funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01 R01AR078268"],"award-info":[{"award-number":["R01 R01AR078268"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01 AI173189-01"],"award-info":[{"award-number":["R01 AI173189-01"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["PATHO-PH2-SUB"],"award-info":[{"award-number":["PATHO-PH2-SUB"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["www.science.org"],"crossmark-restriction":true},"short-container-title":["Sci. Transl. Med."],"published-print":{"date-parts":[[2025,11,12]]},"abstract":"<jats:p>\n                    Systemic lupus erythematosus (SLE) is a systemic autoimmune disease characterized by antinuclear antibodies (ANAs). Epstein-Barr virus (EBV) infection has been epidemiologically associated with SLE, yet its role in pathogenesis remains incompletely defined. Here, we developed an EBV-specific single-cell RNA-sequencing platform and used it to demonstrate that EBV infection reprograms autoreactive antinuclear antigen B cells to drive autoimmunity in SLE. We demonstrated that, in SLE, EBV\n                    <jats:sup>+<\/jats:sup>\n                    B cells are predominantly CD27\n                    <jats:sup>+<\/jats:sup>\n                    CD21\n                    <jats:sup>low<\/jats:sup>\n                    memory B cells that are present at increased frequencies and express\n                    <jats:italic toggle=\"yes\">ZEB2<\/jats:italic>\n                    ,\n                    <jats:italic toggle=\"yes\">TBX21<\/jats:italic>\n                    (T-bet), and antigen-presenting cell transcriptional pathways. Integrative analysis of chromatin immunoprecipitation sequencing (ChIP-seq), assay for transposase-accessible chromatin sequencing (ATAC-seq), and RNA polymerase II occupancy data revealed EBV nuclear antigen 2 (EBNA2) binding at the transcriptional start sites and regulatory regions of\u00a0\n                    <jats:italic toggle=\"yes\">CD27<\/jats:italic>\n                    ,\u00a0\n                    <jats:italic toggle=\"yes\">ZEB2<\/jats:italic>\n                    , and\n                    <jats:italic toggle=\"yes\">TBX21<\/jats:italic>\n                    , as well as the antigen-presenting cell genes demonstrated to be up-regulated in SLE EBV\n                    <jats:sup>+<\/jats:sup>\n                    B cells. We expressed recombinant antibodies from SLE EBV\n                    <jats:sup>+<\/jats:sup>\n                    B cells and demonstrated that they bind prototypical SLE nuclear autoantigens, whereas those from healthy individuals do not. We further found that SLE EBV\n                    <jats:sup>+<\/jats:sup>\n                    B cells can serve as antigen-presenting cells to drive activation of T peripheral helper cells with concomitant activation of related EBV\n                    <jats:sup>\u2212<\/jats:sup>\n                    antinuclear double-negative 2 B cells and plasmablasts. Our results provide a mechanistic basis for EBV being a driver of SLE through infecting and reprogramming nuclear antigen-reactive B cells to become activated antigen-presenting cells with the potential to promote systemic disease\u2013driving autoimmune responses.\n                  <\/jats:p>","DOI":"10.1126\/scitranslmed.ady0210","type":"journal-article","created":{"date-parts":[[2025,11,12]],"date-time":"2025-11-12T18:58:19Z","timestamp":1762973899000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":109,"title":["Epstein-Barr virus reprograms autoreactive B cells as antigen-presenting cells in systemic lupus erythematosus"],"prefix":"10.1126","volume":"17","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4319-1738","authenticated-orcid":true,"given":"Shady","family":"Younis","sequence":"first","affiliation":[{"name":"Division of Immunology and Rheumatology, Stanford University, Stanford, CA 94305, USA."},{"name":"VA Palo Alto Health Care System, Palo Alto, CA 94304, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0001-7206-2185","authenticated-orcid":true,"given":"Salvinaz I.","family":"Moutusy","sequence":"additional","affiliation":[{"name":"Division of Immunology and Rheumatology, Stanford University, Stanford, CA 94305, USA."},{"name":"VA Palo Alto Health Care System, Palo Alto, CA 94304, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9235-0336","authenticated-orcid":true,"given":"Sajede","family":"Rasouli","sequence":"additional","affiliation":[{"name":"Division of Immunology and Rheumatology, Stanford University, Stanford, CA 94305, USA."},{"name":"VA Palo Alto Health Care System, Palo Alto, CA 94304, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7789-4856","authenticated-orcid":true,"given":"Shaghayegh","family":"Jahanbani","sequence":"additional","affiliation":[{"name":"Division of Immunology and Rheumatology, Stanford University, Stanford, CA 94305, USA."},{"name":"VA Palo Alto Health Care System, Palo Alto, CA 94304, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0007-9111-444X","authenticated-orcid":true,"given":"Mahesh","family":"Pandit","sequence":"additional","affiliation":[{"name":"Division of Immunology and Rheumatology, Stanford University, Stanford, CA 94305, USA."},{"name":"VA Palo Alto Health Care System, Palo Alto, CA 94304, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaohao","family":"Wu","sequence":"additional","affiliation":[{"name":"Division of Immunology and Rheumatology, Stanford University, Stanford, CA 94305, USA."},{"name":"VA Palo Alto Health Care System, Palo Alto, CA 94304, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Suman","family":"Acharya","sequence":"additional","affiliation":[{"name":"Division of Immunology and Rheumatology, Stanford University, Stanford, CA 94305, USA."},{"name":"VA Palo Alto Health Care System, Palo Alto, CA 94304, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1986-7555","authenticated-orcid":true,"given":"Orr","family":"Sharpe","sequence":"additional","affiliation":[{"name":"Division of Immunology and Rheumatology, Stanford University, Stanford, CA 94305, USA."},{"name":"VA Palo Alto Health Care System, Palo Alto, CA 94304, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4534-036X","authenticated-orcid":true,"given":"Tilini U.","family":"Wijeratne","sequence":"additional","affiliation":[{"name":"Division of Immunology and Rheumatology, Stanford 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