Anti-DNA antibody subpopulations and lupus nephritis.
As a consequence of increased insight into the cellular and molecular mechanisms responsible for induction of B cell and T cell autoimmunity to DNA and nucleosomes, there is an obvious need to reconsider the dogma stating that anti-dsDNA antibodies serve as marker antibodies for SLE and also that anti-dsDNA antibodies per se are responsible for the initiation of lupus nephritis. Given that the potential to produce anti-dsDNA antibodies is an inherent property of the normal immune system and that few anti-DNA antibodies have nephritogenic potential, we must try to solve the problem whether it is avidity for DNA, specificity for unique DNA structures or cross-reactivity with non-DNA molecules, that make such antibodies pathogenic and thus potential markers for SLE and lupus nephritis. In this review, we will summarize contemporary problems related to these questions; (1) try to focus on phenotypic differences with respect to the ability to produce anti-dsDNA antibodies between individuals suffering from SLE and those not belonging to this diagnostic group, and (2) to describe differences between pathogenic and non-pathogenic anti-dsDNA antibodies.
Department of Biochemistry, Institute of Medical Biology, Faculty of Medicine, University of Tromsø, Tromsø N-9037, Norway. olepr@fagmed.uit.no
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Kalaaji
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D000818:Animals; D000974:Antibodies, Antinuclear / Q000235:genetics / Q000276:immunology*; D000918:Antibody Specificity / Q000235:genetics; D014644:Genetic Variation; D006801:Humans; D007678:Kidney Glomerulus / Q000276:immunology; D008181:Lupus Nephritis / Q000209:etiology / Q000235:genetics / Q000276:immunology*; D009707:Nucleosomes / Q000276:immunology
D000974:Antibodies, Antinuclear; D009707:Nucleosomes