Experimental autologous immune deposit nephritis in rats associated with mercuric chloride administration.
Serial administration of mercuric chloride to rats was followed by development of antibodies to tubular basement membrane and renal tubular epithelial antigen (RTE) and glomerulonephritis characterized by granular deposits of hosts IgG, C3 and RTE along the glomerular capillary walls. The glomerular fixed antibody was directed against RTE. These studies suggest that tubular injury by mercury may lead to release of RTE and autosensitization and subsequent antibody production to this antigen result in formation of and glomerular deposition of circulating immunopathogenic complexes (RTE-anti-RTE) and glomerular morphologic alterations.
D000818:Animals; D001324:Autoantigens / Q000032:analysis; D001327:Autoimmune Diseases / Q000139:chemically induced* / Q000150:complications; D001485:Basement Membrane / Q000276:immunology; D002712:Chlorides; D003176:Complement C3 / Q000032:analysis; D004848:Epithelium / Q000276:immunology; D005455:Fluorescent Antibody Technique; D005921:Glomerulonephritis / Q000209:etiology*; D006651:Histocytochemistry; D007074:Immunoglobulin G / Q000032:analysis; D007684:Kidney Tubules / Q000276:immunology*; D008297:Male; D008628:Mercury; D051381:Rats
D001324:Autoantigens; D002712:Chlorides; D003176:Complement C3; D007074:Immunoglobulin G; D008628:Mercury