Murine lupus nephritis is accelerated by anti-glomerular basement membrane autoantibodies.
We have tested the effect of deposition of non-pathogenic amounts of induced anti-glomerular basement membrane (GBM) autoantibodies on the development of the spontaneous lupus nephritis of female (NZB x NZW) F1 (B x W) mice. Female and male B x W mice were immunized with rabbit renal tubular basement membrane in adjuvant at 2 months of age and their kidneys were examined 35 to 66 days later; control B x W mice were injected with adjuvant only or remained untreated. By immunofluorescent and histopathological criteria, only the 4-month-old female B x W mice with anti-GBM autoantibody deposits had an accelerated onset of lupus nephritis resembling the findings not seen until 6 to 8 months of age in unmanipulated mice. Thus potentially pathogenic amounts of immune complexes are present in young female B x W mice, but these do not deposit in glomeruli until much later in life. Evidently, the anti-GBM autoantibodies modified the glomerular milieu sufficiently to facilitate accelerated immune complex deposition.
D000818:Animals; D001323:Autoantibodies / Q000276:immunology*; D001485:Basement Membrane / Q000276:immunology; D005260:Female; D005455:Fluorescent Antibody Technique; D005921:Glomerulonephritis / Q000276:immunology*; D007074:Immunoglobulin G / Q000032:analysis; D007678:Kidney Glomerulus / Q000276:immunology*; D007684:Kidney Tubules / Q000276:immunology; D008180:Lupus Erythematosus, Systemic / Q000276:immunology*; D008297:Male; D051379:Mice
D001323:Autoantibodies; D007074:Immunoglobulin G