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Immunol."],"published-print":{"date-parts":[[2025,11,14]]},"abstract":"<jats:p>\n                    The extrafollicular (EF) B cell differentiation pathway has emerged as a prominent source of autoantibody-secreting cells (ASCs) in systemic lupus erythematosus (SLE). CD21\n                    <jats:sup>lo<\/jats:sup>\n                    CD11c\n                    <jats:sup>+<\/jats:sup>\n                    B cells are associated with aging, infection, and autoimmunity. They are key contributors to EF ASCs, yet their developmental trajectory and receptor programming are unclear. To study EF mechanics of autoreactive B cells, we adoptively transferred na\u00efve B cell populations into 564Igi mice, which act as an autoreactive host enriched for autoantigens and T cell help. Time-resolved analyses revealed a Toll-like receptor 7 (TLR7)\u2013dependent early escape of peripheral tolerance and a pre\u2013ASC division program. We identified na\u00efve-derived CD21\n                    <jats:sup>lo<\/jats:sup>\n                    cells as precursors of EF ASCs exhibiting elevated reliance on TLR7. Repertoire analysis delineated protoautoreactive B cell selection and receptor evolution toward self-reactivity. Continuous complement receptor 2 (CR2\/CD21)\u2013complement C3d and CD21\u2013complement iC3b engagement triggered receptor down-regulation before proliferation. We reveal CD21 as an initiator of TLR7-dependent autoimmune EF proliferation and target for suppressing autoreactivity.\n                  <\/jats:p>","DOI":"10.1126\/sciimmunol.ads8226","type":"journal-article","created":{"date-parts":[[2025,11,14]],"date-time":"2025-11-14T18:59:21Z","timestamp":1763146761000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":12,"title":["CD21 primes extrafollicular differentiation of autoreactive B cells in a TLR7-driven lupus model"],"prefix":"10.1126","volume":"10","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6327-8673","authenticated-orcid":true,"given":"Danni Y.","family":"Zhu","sequence":"first","affiliation":[{"name":"Program in Cellular and Molecular Medicine, Boston Children\u2019s Hospital, Harvard Medical School, Boston, USA."},{"name":"Harvard Graduate Program in Virology, Boston, USA."},{"name":"Department of Microbiology, Harvard Medical School, Boston, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2074-5416","authenticated-orcid":true,"given":"Daniel P.","family":"Maurer","sequence":"additional","affiliation":[{"name":"Harvard Graduate Program in Virology, Boston, USA."},{"name":"Department of Microbiology, Harvard Medical School, Boston, USA."},{"name":"Ragon Institute of Mass General, MIT, and Harvard, Cambridge, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2909-7371","authenticated-orcid":true,"given":"Carlos","family":"Castrillon","sequence":"additional","affiliation":[{"name":"Department of Medicine, Emory University School of Medicine, Atlanta, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yixiang","family":"Deng","sequence":"additional","affiliation":[{"name":"Ragon Institute of Mass General, MIT, and Harvard, Cambridge, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Faez A. 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