{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,6]],"date-time":"2026-02-06T00:38:52Z","timestamp":1770338332483,"version":"3.49.0"},"reference-count":27,"publisher":"Oxford University Press (OUP)","issue":"5","license":[{"start":{"date-parts":[[2008,9,1]],"date-time":"2008-09-01T00:00:00Z","timestamp":1220227200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2008,9,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>MRL\/lpr mice develop a spontaneous systemic lupus erythematosus-like autoimmune syndrome due to a dysfunctional Fas receptor, with contributions from other less well-defined genetic loci. The removal of B cells by genetic manipulation not only prevents autoantibody formation, but it also results in substantially reduced T cell activation and kidney inflammation. To determine whether B cell depletion by administration of Abs is effective in lupus mice with an intact immune system and established disease, we screened several B cell-specific mAbs and found that a combination of anti-CD79\u03b1 and anti-CD79\u03b2 Abs was most effective at depleting B cells in vivo. Anti-CD79 therapy started at 4\u20135 mo of age in MRL\/lpr mice significantly decreased B cells (B220+CD19+) in peripheral blood, bone marrow, and spleens. Treated mice also had a significant increase in the number of both double-negative T cells and naive CD4+ T cells, and a decreased relative abundance of CD4+ memory cells. Serum anti-chromatin IgG levels were significantly decreased compared with controls, whereas serum anti-dsDNA IgG, total IgG, or total IgM were unaffected. Overall, survival was improved with lower mean skin scores and significantly fewer focal inflammatory infiltrates in submandibular salivary glands and kidneys. Anti-CD79 mAbs show promise as a potential treatment for systemic lupus erythematosus and as a model for B cell depletion in vivo.<\/jats:p>","DOI":"10.4049\/jimmunol.181.5.2961","type":"journal-article","created":{"date-parts":[[2014,4,18]],"date-time":"2014-04-18T19:32:15Z","timestamp":1397849535000},"page":"2961-2972","source":"Crossref","is-referenced-by-count":50,"title":["B Cell Depletion with Anti-CD79 mAbs Ameliorates Autoimmune Disease in MRL\/\n                    <i>lpr<\/i>\n                    Mice"],"prefix":"10.1093","volume":"181","author":[{"given":"Yongmei","family":"Li","sequence":"first","affiliation":[{"name":"Division of Rheumatology, Department of Medicine, University of Pennsylvania , Philadelphia, PA 19104"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Fangqi","family":"Chen","sequence":"additional","affiliation":[{"name":"Division of Rheumatology, Department of Medicine, University of Pennsylvania , Philadelphia, PA 19104"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mary","family":"Putt","sequence":"additional","affiliation":[{"name":"Department of Biostatistics and Epidemiology, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania , Philadelphia, PA 19104"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yumee K","family":"Koo","sequence":"additional","affiliation":[{"name":"Department of Chemistry and Biochemistry, University of Sciences in Philadelphia , Philadelphia, PA 19104"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Michael","family":"Madaio","sequence":"additional","affiliation":[{"name":"Temple University , Philadelphia, PA 19140"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"John C","family":"Cambier","sequence":"additional","affiliation":[{"name":"University of Colorado Denver School of Medicine and National Jewish Medical and Research Center , Denver, CO 80206"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Philip L","family":"Cohen","sequence":"additional","affiliation":[{"name":"Division of Rheumatology, Department of Medicine, University of Pennsylvania , Philadelphia, PA 19104"},{"name":"Philadelphia Veterans Affairs Medical Center , Philadelphia, PA 19104"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Robert A","family":"Eisenberg","sequence":"additional","affiliation":[{"name":"Division of Rheumatology, Department of Medicine, University of Pennsylvania , Philadelphia, PA 19104"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2008,9,1]]},"reference":[{"key":"2026012806255641800_R1","first-page":"1583","article-title":"Role of B cells as antigen-presenting cells in vivo revisited: antigen-specific B cells are essential for T cell expansion in lymph nodes and for systemic T cell responses to low antigen concentrations","volume-title":"Int. Immunol.","year":"2001"},{"key":"2026012806255641800_R2","first-page":"764","article-title":"Systemic lupus erythematosus: an autoimmune disease of B cell hyperactivity","volume-title":"Nat. Immunol.","year":"2001"},{"key":"2026012806255641800_R3","first-page":"19","article-title":"B lymphocytes are required for development and treatment of autoimmune diseases","volume-title":"Ann. NY Acad. Sci.","year":"2005"},{"key":"2026012806255641800_R4","first-page":"25","article-title":"Regulatory roles for cytokine-producing B cells in infection and autoimmune disease","volume-title":"Curr. Dir. Autoimmun.","year":"2005"},{"key":"2026012806255641800_R5","first-page":"1658","article-title":"Cutting edge: B cells promote CD8+ T cell activation in MRL-Faslpr mice independently of MHC class I antigen presentation","volume-title":"J. 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Immunol.","year":"1993"},{"key":"2026012806255641800_R19","first-page":"1537","article-title":"TCR-induced transmembrane signaling by peptide\/MHC class II via associated Ig-\u03b1\/\u03b2 dimers","volume-title":"Science","year":"2001"},{"key":"2026012806255641800_R20","first-page":"7913","article-title":"Analysis of the individual contributions of Ig\u03b1 (CD79a)- and Ig\u03b2 (CD79b)-mediated tonic signaling for bone marrow B cell development and peripheral B cell maturation","volume-title":"J. Immunol.","year":"2006"},{"key":"2026012806255641800_R21","first-page":"747","article-title":"IgG1 B cell receptor signaling is inhibited by CD22 and promotes the development of B cells whose survival is less dependent on Ig\u03b1\/\u03b2","volume-title":"J. Exp. 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