Influence of avidity of circulating anti-DNA antibodies on murine lupus nephritis.
We determined the avidity of antiDNA antibodies in plasma of NZB/W mice when nephritis became apparent, when such mice developed chronic glomerulonephritis, and in mice whose nephritis was arrested, or attenuated, by immunosuppression. Antibody avidity was estimated by the rate of dissociation of 125IDNA-antiDNA complexes when excess unlabelled DNA was added to the plasma. In all groups of mice studied, the relative contributions of high and low avidity antiDNA antibodies were comparable and, overall, high avidity antibodies predominated. The results indicate that the avidity of circulating antiDNA antibodies did not reflect the extent and type of glomerular involvement, and was not predictive of clinical course.
D000818:Animals; D000915:Antibody Affinity; D001323:Autoantibodies / Q000276:immunology*; D001379:Azathioprine / Q000494:pharmacology; D003520:Cyclophosphamide / Q000494:pharmacology; D004247:DNA / Q000276:immunology*; D005260:Female; D007165:Immunosuppression Therapy; D008180:Lupus Erythematosus, Systemic / Q000150:complications / Q000188:drug therapy / Q000276:immunology*; D008775:Methylprednisolone / Q000494:pharmacology; D051379:Mice; D008814:Mice, Inbred NZB; D009393:Nephritis / Q000150:complications / Q000276:immunology*
D001323:Autoantibodies; D003520:Cyclophosphamide; D004247:DNA; D001379:Azathioprine; D008775:Methylprednisolone