Pathogenesis of the glomerulonephritis of NZB/W mice.
The development of glomerulonephritis in NZB/W mice is closely related to the formation of antinuclear, particularly anti-DNA, antibodies. The developing inflammatory glomerular lesions are characterized by the deposition of gammaG- and beta(1C)-globulins plus DNA and possibly other nuclear antigens, presumably as complexes, in a granular to lumpy pattern along the capillary walls and in the mesangia. Elution studies revealed the gammaG-globulin in the glomeruli to be largely gammaG(2A)-type antibody to soluble nuclear antigens. Enhancement of the antinuclear antibody response by active immunization of young NZB/W mice with DNA-methylated BSA hastens the development and increases the severity of the glomerulonephritis. Similarly, injections of soluble DNA into NZB/W mice with circulating anti-DNA antibodies but with as yet little nephritis causes rapid progression of nephritis.
D000818:Animals; D000974:Antibodies, Antinuclear / Q000032:analysis; D000917:Antibody Formation; D000937:Antigen-Antibody Reactions; D000941:Antigens; D003168:Complement Fixation Tests; D004247:DNA; D005260:Female; D005455:Fluorescent Antibody Technique; D005921:Glomerulonephritis / Q000209:etiology / Q000276:immunology* / Q000473:pathology; D005779:Immunodiffusion; D008297:Male; D051379:Mice; D009698:Nucleoproteins; D011507:Proteinuria / Q000209:etiology; D005719:gamma-Globulins / Q000032:analysis
D000974:Antibodies, Antinuclear; D000941:Antigens; D009698:Nucleoproteins; D005719:gamma-Globulins; D004247:DNA