Passive Heymann's nephritis as a model of immune glomerulonephritis mediated  by antibodies to immunoglobulins.
The autologous phase of passive Heymann's nephritis (PHN) induced in rats by a single injection of rabbit IgG anti-FxlA has been investigated. Tolerance to normal rabbit IgG prior to induction of PHN abolished or strongly diminished the glomerular deposition of the host's IgG during the early autologous phase and prevented the development of proteinuria. Neonatal thymectomy significantly decreased the anti-rabbit IgG response but did not prevent the development and the progression of glomerulopathy. Passive transfer of rat or sheep anti-rabbit IgG hyperimmune serum during the heterologous phase resulted in an earlier accumulation of the injected IgG along the glomerular capillary walls (GCW). These results demonstrate the importance of the host's humoral immune response to the injected rabbit IgG anti-FxlA antibody in the progression and in the maintenance of glomerular immune lesions.
D000818:Animals; D000888:Antibodies, Anti-Idiotypic / Q000096:biosynthesis; D005455:Fluorescent Antibody Technique; D005921:Glomerulonephritis / Q000276:immunology*; D007108:Immune Tolerance; D007116:Immunization, Passive; D007074:Immunoglobulin G / Q000276:immunology*; D007668:Kidney / Q000276:immunology; D007678:Kidney Glomerulus / Q000276:immunology; D008297:Male; D011817:Rabbits / Q000276:immunology; D051381:Rats; D011917:Rats, Inbred Lew; D013934:Thymectomy
D000888:Antibodies, Anti-Idiotypic; D007074:Immunoglobulin G