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Immunological tolerance to MR16-1 or isotype-matched control antibody, KH-5, was induced by the simultaneous administration of anti-CD4 MoAb in mice. Thereafter, mice were intraperitoneally given 0.5\u2003mg of MR16-1, 0.5\u2003mg of KH-5 or saline once a week from 13 to 64 weeks of age. MR16-1 treatment dramatically suppressed proteinuria and prolonged the survival time of BWF1 mice. Only one out of 10 mice died with high levels of proteinuria throughout the experiment. MR16-1 almost completely suppressed the production of IgG forms of anti-DNA and anti-TNP antibodies, but not the IgM forms of these antibodies. In particular, all IgG subclasses (IgG1, IgG2a, IgG2b and IgG3) of anti-DNA antibody production were significantly suppressed. Moreover, serum IgG1, IgG2a and IgG3 levels in MR16-1-treated mice were lower than those in saline- and KH-5-treated mice, whereas serum IgM and IgA levels were not influenced. In conclusion, MR16-1 potently suppressed the development of autoimmune disease in BWF1 mice, and this was attributed to its effect of specific suppression of IgG class antibody production.<\/jats:p>","DOI":"10.1046\/j.1365-2249.1998.00612.x","type":"journal-article","created":{"date-parts":[[2003,3,11]],"date-time":"2003-03-11T10:11:12Z","timestamp":1047377472000},"page":"397-402","source":"Crossref","is-referenced-by-count":123,"title":["IL-6 receptor blockage inhibits the onset of autoimmune kidney disease in NZB\/W F1 mice"],"prefix":"10.1093","volume":"112","author":[{"given":"M","family":"Mihara","sequence":"first","affiliation":[{"name":"Fuji-Gotemba Research Laboratories, Chugai Pharmaceutical Co. Ltd, Shizuoka, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"N","family":"Takagi","sequence":"additional","affiliation":[{"name":"Fuji-Gotemba Research Laboratories, Chugai Pharmaceutical Co. 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