{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,18]],"date-time":"2026-09-18T18:34:23Z","timestamp":1789756463539,"version":"4.0.1"},"reference-count":80,"publisher":"Oxford University Press (OUP)","issue":"4","license":[{"start":{"date-parts":[[2006,8,1]],"date-time":"2006-08-01T00:00:00Z","timestamp":1154390400000},"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":[[2006,8,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Constitutive overexpression of B cell-activating factor belonging to the TNF family (BAFF) promotes development of systemic lupus erythematosus (SLE), and treatment of SLE mice with BAFF antagonists ameliorates disease. To determine whether SLE can develop de novo in BAFF-deficient hosts, BAFF-deficient New Zealand Mixed (NZM) 2328 (NZM.Baff\u2212\/\u2212) mice were generated. In NZM.Baff\u2212\/\u2212 mice, spleen B cells (including CD5+ B1a and CD5\u2212 B1b B cells), germinal centers, Ig-secreting cells, and T cells were reduced in comparison to NZM.Baff+\/+ mice. Serum total Ig and autoantibody levels were reduced at 4\u20136 mo but approached wild-type levels with increasing age, indicating that autoreactive B cells can survive and secrete autoantibodies despite the complete absence of BAFF. At least some of these autoantibodies are nephrophilic in that glomerular deposition of total IgG and IgG1 (but not of IgG2a, IgG2b, or C3) was substantial in NZM.Baff\u2212\/\u2212 mice by 12\u201313 mo of age. Despite proliferative glomerulonephritis, highlighted by widespread glomerular hyaline thrombi, being common among NZM.Baff\u2212\/\u2212 mice by 6\u20137 mo of age, severe proteinuria and mortality were greatly attenuated. These results demonstrate that the lifelong absence of BAFF does not protect NZM 2328 mice from serological autoimmunity and renal pathology. Nevertheless, the character of the renal pathology is altered, and the mice are largely spared from clinically overt disease (severe proteinuria and premature death). These observations may have profound ramifications for the use of BAFF antagonists in human SLE and related diseases.<\/jats:p>","DOI":"10.4049\/jimmunol.177.4.2671","type":"journal-article","created":{"date-parts":[[2014,4,18]],"date-time":"2014-04-18T23:20:43Z","timestamp":1397863243000},"page":"2671-2680","source":"Crossref","is-referenced-by-count":93,"title":["Paucity of Clinical Disease despite Serological Autoimmunity and Kidney Pathology in Lupus-Prone New Zealand Mixed 2328 Mice Deficient in BAFF"],"prefix":"10.1093","volume":"177","author":[{"given":"Chaim O","family":"Jacob","sequence":"first","affiliation":[{"name":"Department of Medicine, University of Southern California Keck School of Medicine , Los Angeles, CA 90033"},{"name":"Division of Gastrointestinal and Liver Diseases, University of Southern California Keck School of Medicine , Los Angeles, CA 90033"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Luminita","family":"Pricop","sequence":"additional","affiliation":[{"name":"Department of Medicine, Hospital for Special Surgery, Weill Medical College of Cornell University , New York, NY 10021"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chaim","family":"Putterman","sequence":"additional","affiliation":[{"name":"Division of Rheumatology, Albert Einstein College of Medicine , Bronx, NY 10461"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael N","family":"Koss","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Southern California Keck School of Medicine , Los Angeles, CA 90033"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yi","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Medicine, Hospital for Special Surgery, Weill Medical College of Cornell University , New York, NY 10021"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maria","family":"Kollaros","sequence":"additional","affiliation":[{"name":"Division of Rheumatology, Albert Einstein College of Medicine , Bronx, NY 10461"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sarah A","family":"Bixler","sequence":"additional","affiliation":[{"name":"Research Department, Biogen Idec , Cambridge, MA 02142"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christine M","family":"Ambrose","sequence":"additional","affiliation":[{"name":"Research Department, Biogen Idec , Cambridge, MA 02142"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Martin L","family":"Scott","sequence":"additional","affiliation":[{"name":"Research Department, Biogen Idec , Cambridge, MA 02142"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"William","family":"Stohl","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Southern California Keck School of Medicine , Los Angeles, CA 90033"},{"name":"Division of Rheumatology, University of Southern California Keck School of Medicine , Los Angeles, CA 90033"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2006,8,15]]},"reference":[{"key":"2025032807262292100_R1","first-page":"1747","volume-title":"J. 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