{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,31]],"date-time":"2026-01-31T03:50:44Z","timestamp":1769831444750,"version":"3.49.0"},"reference-count":75,"publisher":"Oxford University Press (OUP)","issue":"8","license":[{"start":{"date-parts":[[2011,4,1]],"date-time":"2011-04-01T00:00:00Z","timestamp":1301616000000},"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":[[2011,4,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>IFN-\u03b1 is a potent activator of innate and adaptive immunity, and its administration to preautoimmune (NZB\u00d7NZW)F1 mice promotes virulent systemic lupus erythematosus (SLE) disease. Given the known contributions of B cells and BAFF to SLE, we evaluated the ability of IFN-\u03b1 administration to induce disease in wild-type (WT), B cell-deficient, and BAFF-deficient NZM 2328 mice. Whereas WT mice rapidly developed proliferative glomerulonephritis, marked proteinuria, and increased mortality in response to IFN-\u03b1 administration, B cell-deficient mice developed neither renal pathology nor clinical disease. Moreover, BAFF-deficient mice, despite developing limited glomerular IgG and C3 deposition, also remained free of histological glomerulonephritis and clinical disease. Strikingly, similar T cell expansion and serum IgG responses were observed in adenovirus (Adv)-IFN\u2013treated WT and BAFF-deficient mice despite their disparate pathological and clinical responses, whereas numbers of activated B cells increased in WT mice but not in BAFF-deficient mice. Nonetheless, B cell, plasma cell, and T cell infiltration of the kidneys in Adv-IFN\u2013treated WT mice was similar to that in WT mice treated with Adv-control. Its ability to promote SLE disease in WT mice notwithstanding, IFN-\u03b1 administration failed to drive the preferential expansion of CD4+ memory T cells that occurs during the natural course of disease, and glomerular infiltration of macrophages failed to associate with development of disease. These results collectively suggest that therapeutic targeting in SLE of BAFF and\/or B cells in SLE could be successful even in states of IFN-\u03b1 overexpression. Moreover, our results document important biological differences between IFN-\u03b1\u2013driven and spontaneous natural SLE disease.<\/jats:p>","DOI":"10.4049\/jimmunol.1000466","type":"journal-article","created":{"date-parts":[[2011,3,8]],"date-time":"2011-03-08T12:54:42Z","timestamp":1299588882000},"page":"4984-4993","source":"Crossref","is-referenced-by-count":73,"title":["B Cell and BAFF Dependence of IFN-\u03b1\u2013Exaggerated Disease in Systemic Lupus Erythematosus-Prone NZM 2328 Mice"],"prefix":"10.1093","volume":"186","author":[{"given":"Noam","family":"Jacob","sequence":"first","affiliation":[{"name":"Division of Rheumatology, University of Southern California Keck School of Medicine , Los Angeles, CA 90033"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shunhua","family":"Guo","sequence":"additional","affiliation":[{"name":"Division of Rheumatology, University of Southern California Keck School of Medicine , Los Angeles, CA 90033"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Alexis","family":"Mathian","sequence":"additional","affiliation":[{"name":"Service de M\u00e9decine Interne 2, Centre Hospitalier de l\u2019Universit\u00e9 Piti\u00e9-Salp\u00eatri\u00e8re, Assistance Publique-H\u00f4pitaux de Paris , 75651 Paris Cedex 13 ,","place":["France"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"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":[{"role":"author","vocabulary":"crossref"}]},{"given":"Simona","family":"Gindea","sequence":"additional","affiliation":[{"name":"Division of Rheumatology, Albert Einstein College of Medicine , Bronx, NY 10461"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Chaim","family":"Putterman","sequence":"additional","affiliation":[{"name":"Division of Rheumatology, Albert Einstein College of Medicine , Bronx, NY 10461"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Chaim O","family":"Jacob","sequence":"additional","affiliation":[{"name":"Division of Gastrointestinal and Liver Diseases, University of Southern California Keck School of Medicine , Los Angeles, CA 90033"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"William","family":"Stohl","sequence":"additional","affiliation":[{"name":"Division of Rheumatology, University of Southern California Keck School of Medicine , Los Angeles, CA 90033"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2011,4,15]]},"reference":[{"key":"2025032411211218700_r1","doi-asserted-by":"crossref","first-page":"8661","DOI":"10.1073\/pnas.88.19.8661","article-title":"Enforced BCL2 expression in B-lymphoid cells prolongs antibody responses and elicits autoimmune disease","volume":"88","author":"Strasser","year":"1991","journal-title":"Proc. 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