{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T05:36:44Z","timestamp":1791351404074,"version":"4.3.1"},"reference-count":40,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2005,12,29]],"date-time":"2005-12-29T00:00:00Z","timestamp":1135814400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Arthritis &amp; Rheumatism"],"published-print":{"date-parts":[[2006,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Objective<\/jats:title><jats:p>C\u2010reactive protein (CRP) is an acute\u2010phase serum protein with binding reactivity to nuclear autoantigens and immunomodulatory function. The MRL\/<jats:italic>lpr<\/jats:italic> mouse is an important model of human systemic lupus erythematosus (SLE). These mice develop high\u2010titer anti\u2010DNA antibodies and immune complex\u2013mediated nephritis and exhibit progressive lymphadenopathy. The mortality rate among these mice is 50% by age 18\u201320 weeks; the most frequent cause of death is glomerulonephritis. The present study was undertaken to determine whether treatment of mice with CRP would affect the course of lupus nephritis.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>MRL\/<jats:italic>lpr<\/jats:italic> mice were treated with a single 200\u2010\u03bcg injection of CRP at either age 6 weeks (before disease onset) or age 13 or 15 weeks (when proteinuria had reached high levels). Proteinuria was measured weekly, and levels of anti\u2013double\u2010stranded DNA autoantibodies and blood urea nitrogen were determined monthly. Glomerular immune complex deposition and renal pathology were assessed in mice ages 15 weeks and 17 weeks.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Early CRP treatment markedly delayed the onset of proteinuria and lymphadenopathy, increased survival, and reduced levels of autoantibodies to DNA. Treatment of mice with active disease reversed proteinuria and prolonged survival. Renal disease was decreased in CRP\u2010treated mice, with a marked suppression of glomerular pathology, tubular degeneration, and interstitial inflammation, which correlated with the decrease in proteinuria and azotemia.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>These findings demonstrate that systemic suppression of autoimmunity is initiated by a single injection of CRP. Long\u2010term maintenance of CRP\u2010mediated protection was reversed by injection of an anti\u2010CD25 monoclonal antibody but not by macrophage depletion, suggesting that disease suppression is maintained by CD25\u2010bearing T cells.<\/jats:p><\/jats:sec>","DOI":"10.1002\/art.21556","type":"journal-article","created":{"date-parts":[[2005,12,29]],"date-time":"2005-12-29T19:16:39Z","timestamp":1135883799000},"page":"325-335","source":"Crossref","is-referenced-by-count":75,"title":["Prevention and reversal of nephritis in MRL\/<i>lpr<\/i> mice with a single injection of C\u2010reactive protein"],"prefix":"10.1002","volume":"54","author":[{"given":"Wilfredo","family":"Rodriguez","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carolyn","family":"Mold","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lorraine 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