{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T22:19:08Z","timestamp":1790461148284,"version":"4.1.0"},"reference-count":52,"publisher":"National Academy of Sciences","issue":"22","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2010,6]]},"abstract":"<jats:p>\n                    Interferon regulatory factor (IRF) 5 is a key transcription factor for the activation of innate immune responses downstream of Toll-like receptor signaling. Based on recent genetic analyses, IRF5 is a focus for its potential involvement in systemic lupus erythematosus (SLE), although how IRF5 contributes to SLE is uncertain. In this study, we demonstrate a requirement for IRF5 in the development of murine SLE via its role in B lymphocytes. We show that antinuclear autoantibodies and Ig glomerular deposits, hallmarks of SLE, are absent in\n                    <jats:italic>\n                      Irf5\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    <\/jats:italic>\n                    mice challenged to develop SLE by pristane injection. In particular, production of autoantibodies of the IgG2a subtype, the most prominent isotype in inducing autoimmunity, requires IRF5. Finally, we provide evidence for the critical role of this transcription factor in the secretion of pathogenic antibodies through its direct control of class switch recombination of the \u03b32a locus. By demonstrating a B-cell-intrinsic role, this study places IRF5 in a context that may have implications for understanding the pathogenesis of human SLE.\n                  <\/jats:p>","DOI":"10.1073\/pnas.1005599107","type":"journal-article","created":{"date-parts":[[2010,5,17]],"date-time":"2010-05-17T22:13:23Z","timestamp":1274134403000},"page":"10154-10159","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":101,"title":["Contribution of IRF5 in B cells to the development of murine SLE-like disease through its transcriptional control of the IgG2a locus"],"prefix":"10.1073","volume":"107","author":[{"given":"David A.","family":"Savitsky","sequence":"first","affiliation":[{"name":"Department of Immunology, Graduate School of Medicine and Faculty of Medicine, University of Tokyo, Bunkyo-ku, Tokyo 113-0031, Japan;"},{"name":"Core Research for Evolution Science and Technology, Japan Science and Technology Agency, Chiyoda-ku, Tokyo 102-0075, Japan;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hideyuki","family":"Yanai","sequence":"additional","affiliation":[{"name":"Department of Immunology, Graduate School of Medicine and Faculty of Medicine, University of Tokyo, Bunkyo-ku, Tokyo 113-0031, Japan;"},{"name":"Core Research for Evolution Science and Technology, Japan Science and Technology Agency, Chiyoda-ku, Tokyo 102-0075, Japan;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tomohiko","family":"Tamura","sequence":"additional","affiliation":[{"name":"Department of Immunology, Graduate School of Medicine and Faculty of Medicine, University of Tokyo, Bunkyo-ku, Tokyo 113-0031, Japan;"},{"name":"Graduate School of Medicine and Faculty of Medicine, Yokohama City University, Kanazawa-ku, Yokohama, Kanagawa 236-0004, Japan; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tadatsugu","family":"Taniguchi","sequence":"additional","affiliation":[{"name":"Department of Immunology, Graduate School of Medicine and Faculty of Medicine, University of Tokyo, Bunkyo-ku, Tokyo 113-0031, Japan;"},{"name":"Core Research for Evolution Science and Technology, Japan Science and Technology Agency, Chiyoda-ku, Tokyo 102-0075, Japan;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kenya","family":"Honda","sequence":"additional","affiliation":[{"name":"Department of Immunology, Graduate School of Medicine and Faculty of Medicine, University of Tokyo, Bunkyo-ku, Tokyo 113-0031, Japan;"},{"name":"Precursory Research for Embryonic Science and Technology, Japan Science and Technology Agency, Saitama 332-0012, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"341","published-online":{"date-parts":[[2010,5,17]]},"reference":[{"key":"e_1_3_3_1_2","doi-asserted-by":"publisher","DOI":"10.1016\/S1074-7613(04)00112-8"},{"key":"e_1_3_3_2_2","first-page":"182","article-title":"B cell biology and dysfunction in SLE","volume":"65","author":"Anolik JH","year":"2007","unstructured":"JH Anolik, B cell biology and dysfunction in SLE. 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