Mercuric chloride induced autoimmune disease in Brown-Norway rats: sequential search for anti-basement membrane antibodies and circulating immune complexes

• Published in: European journal of clinical investigation Vol. 12; no. 2; p. 127
• Main Authors: Bellon, B, Capron, M, Druet, E, Verroust, P, Vial, M C, Sapin, C, Girard, J F, Foidart, J M, Mahieu, P, Druet, P
• Format: Journal Article
• Language: English
• Published: England 01.04.1982
• Subjects: Animals; Antigen-Antibody Complex - analysis; Autoantibodies - analysis; Autoantibodies - biosynthesis; Autoimmune Diseases - chemically induced; Autoimmune Diseases - immunology; Basement Membrane - immunology; Basement Membrane - pathology; Complement Activating Enzymes - metabolism; Complement C1q; Complement System Proteins - analysis; Female; Glycoproteins - immunology; Immunoglobulin G; Kidney Glomerulus - immunology; Kidney Glomerulus - pathology; Laminin; Male; Mercuric Chloride; Mercury; Rats; Rats, Inbred BN; Receptors, Complement; Time Factors
• ISSN: 0014-2972; 1365-2362
• DOI: 10.1111/j.1365-2362.1982.tb00949.x

Mercuric chloride induces in the Brown-Norway rat a biphasic autoimmune disease characterized initially by linear IgG deposits along the glomerular basement membrane followed later by granular IgG deposition. In the present study, anti-glomerular basement membrane antibodies and immune complex-like material were sequentially assessed in serial serum samples. Both were transiently found at the same period. Glomerular linear IgG deposits were present on day 11 but circulating anti-glomerular basement membrane antibodies were only found later on day 16. Circulating immune complexes were first detectable on day 8 before the earliest granular IgG deposits were first observed in the spleen vessels on day 16. The disappearance of circulating anti-glomerular basement membrane antibodies and of circulating immune complexes, although HgCl2 injections were pursued, is in agreement with the self-limited character of mercuric chloride induced autoimmune disease and suggests the induction of immunosuppressive mechanisms.