{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T11:53:27Z","timestamp":1791114807601,"version":"4.1.0"},"reference-count":29,"publisher":"Oxford University Press (OUP)","issue":"3","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":[[2006,8,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>An increasing number of studies indicate that a subset of CD4+ T cells with regulatory capacity (regulatory T cells; Tregs) can function to control organ-specific autoimmune disease. To determine whether abnormalities of thymic-derived Tregs play a role in systemic lupus erythematosus, we evaluated Treg prevalence and function in (New Zealand Black \u00d7 New Zealand White)F1 (B\/W) lupus-prone mice. To explore the potential of Tregs to suppress disease, we evaluated the effect of adoptive transfer of purified, ex vivo expanded thymic-derived Tregs on the progression of renal disease. We found that although the prevalence of Tregs is reduced in regional lymph nodes and spleen of prediseased B\/W mice compared with age-matched non-autoimmune mice, these cells increase in number in older diseased mice. In addition, the ability of these cells to proliferate in vitro was comparable to those purified from non-autoimmune control animals. Purified CD4+CD25+CD62Lhigh B\/W Tregs were expanded ex vivo 80-fold, resulting in cells with a stable suppressor phenotype. Adoptive transfer of these exogenously expanded cells reduced the rate at which mice developed renal disease; a second transfer after treated animals had developed proteinuria further slowed the progression of renal disease and significantly improved survival. These studies indicate that thymic-derived Tregs may have a significant role in the control of autoimmunity in lupus-prone B\/W mice, and augmentation of these cells may constitute a novel therapeutic approach for systemic lupus erythematosus.<\/jats:p>","DOI":"10.4049\/jimmunol.177.3.1451","type":"journal-article","created":{"date-parts":[[2014,4,24]],"date-time":"2014-04-24T16:59:02Z","timestamp":1398358742000},"page":"1451-1459","source":"Crossref","is-referenced-by-count":229,"title":["Suppression of Disease in New Zealand Black\/New Zealand White Lupus-Prone Mice by Adoptive Transfer of Ex Vivo Expanded Regulatory T Cells"],"prefix":"10.1093","volume":"177","author":[{"given":"Kenneth J","family":"Scalapino","sequence":"first","affiliation":[{"name":"Department of Medicine, Division of Rheumatology, University of California San Francisco and San Francisco Veterans Affairs Medical Center , San Francisco, CA 94121"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qizhi","family":"Tang","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of California San Francisco Diabetes Center, University of California San Francisco , San Francisco, CA 94121"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jeffrey A","family":"Bluestone","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of California San Francisco Diabetes Center, University of California San Francisco , San Francisco, CA 94121"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mark L","family":"Bonyhadi","sequence":"additional","affiliation":[{"name":"Xcyte , Seattle, WA 98104"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David I","family":"Daikh","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Rheumatology, University of California San Francisco and San Francisco Veterans Affairs Medical Center , San Francisco, CA 94121"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2006,8,1]]},"reference":[{"key":"2025032807160002600_R1","first-page":"5317","volume-title":"J. 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