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Work from our laboratory and from other investigators shows that antinuclear, antihistone or anti\u2010dsDNA antibodies are neither required nor sufficient for development of lupus GN. In addition, antibody to dsDNA can be generated by mechanisms other than loss of tolerance to chromatin. Genetic analyses demonstrate that although there is some interaction between autoantibody production and renal disease, the phenotypes are regulated by distinct genetic intervals. Furthermore, renal failure is not an essential outcome of the immune\u2010complex deposition and proliferative lupus GN. These data are also supported by published studies from systemic lupus erythematosus (SLE) patients. The immune regulation of lupus GN is distinct from other organ\u2010specific diseases and not influenced by CD25<jats:sup>+<\/jats:sup> or NK1.1<jats:sup>+<\/jats:sup> regulatory T cells. Thus, fatal GN may depend upon a kidney\u2010reactive T\u2010cell response that, in turn, may be regulated by gender and intrinsic end\u2010organ factors. The data discussed in this review call for a re\u2010evaluation of the current paradigms for pathogenesis of SLE. An interactive model separating autoimmunity from end\u2010organ susceptibility for the pathogenesis of SLE is proposed.<\/jats:p>","DOI":"10.1111\/j.0300-9475.2004.01463.x","type":"journal-article","created":{"date-parts":[[2004,7,5]],"date-time":"2004-07-05T19:20:35Z","timestamp":1089055235000},"page":"52-63","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":27,"title":["Lupus Glomerulonephritis Revisited 2004: Autoimmunity and End\u2010Organ Damage"],"prefix":"10.1111","volume":"60","author":[{"given":"H.","family":"Bagavant","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"U. 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