Glomerular and vascular IgG deposits in HgCl2 nephritis: role of circulating antibodies and of immune complexes.
The respective roles of circulating anti-glomerular basement membrane antibodies and of circulating immune complexes in the appearance of glomerular linear and granular IgG deposition during HgCl2-induced glomerulonephritis in the Brown-Norway rat has been studied. Syngeneic kidney transplantations have been performed at various phases of the disease. Results show that circulating antibodies are responsible for linear IgG deposition which did not change to granular deposits during the course of the disease. Electron-dense subepithelial deposits occurred only when circulating immune complexes were detected. These experiments strongly suggest that, in the mercury model, circulating immune complexes are responsible for granular IgG deposits observed in arteries and in the subepithelial space of glomeruli.
D000818:Animals; D000906:Antibodies / Q000276:immunology*; D000936:Antigen-Antibody Complex / Q000276:immunology*; D001485:Basement Membrane / Q000276:immunology; D001706:Biopsy; D007074:Immunoglobulin G / Q000032:analysis*; D007668:Kidney / Q000473:pathology; D007678:Kidney Glomerulus / Q000276:immunology*; D016030:Kidney Transplantation; D008297:Male; D008627:Mercuric Chloride; D008628:Mercury; D009393:Nephritis / Q000139:chemically induced / Q000276:immunology*; D051381:Rats; D011919:Rats, Inbred Strains
D000906:Antibodies; D000936:Antigen-Antibody Complex; D007074:Immunoglobulin G; D008627:Mercuric Chloride; D008628:Mercury