Immune complex type disease induced by HgCl2 in Brown-Norway rats: genetic control of susceptibility.
Mercuric chloride induces a biphasic autoimmune glomerulonephritis in Brown-Norway (BN) rats but not in Lewis (LEW) rats. The genetic control of susceptibility to both phases was investigated by testing the response of segregants between BN and LEW rats and of congenic LEW.1N rats. It was confirmed that susceptibility to the first phase, characterized by the appearance of anti-glomerular basement membrane antibodies, depends on several genes one of which is RT1 linked. Susceptibility to the second phase, which is an immune complex type glomerulonephritis, was found to depend on one major RT1 linked gene or cluster of genes with a role for other(s) non-RT1 linked gene(s) controlling the magnitude of the response. However, congenic LEW.1N rats were found to be resistant. This suggests that the disease gene has been lost during the strain derivation. The question of whether both phases are two different diseases or expression of the same process cannot be definitely answered; data however indicate a dissociation of both disease processes.
D000818:Animals; D000917:Antibody Formation; D001485:Basement Membrane / Q000276:immunology; D005260:Female; D005921:Glomerulonephritis / Q000139:chemically induced / Q000235:genetics* / Q000276:immunology; D007105:Immune Complex Diseases / Q000139:chemically induced / Q000235:genetics*; D007678:Kidney Glomerulus / Q000276:immunology; D008297:Male; D008627:Mercuric Chloride; D008628:Mercury; D051381:Rats; D011914:Rats, Inbred BN; D011917:Rats, Inbred Lew
D008627:Mercuric Chloride; D008628:Mercury