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Nephrol Dial Transplant (1993) 8: 122-127
© 1993 European Renal Association-European Dialysis and Transplant Association

research-article

Evidence for a role of antilaminin-producing B cell clones that escape tolerance in the pathogenesis of HgCl2-induced membranous glomerulopathy

Ph. Icard1, L. Pelletier2,, M.-C. Vial2, C. Mandet2, R. Pasquier2, A. Michel1 and Ph. Druet2

1Laboratoire de recherches chirurgicales, Hôopital Cochin 2INSERM U28, Hopital Broussais Paris, France

Correspondence and offprint requests to: Correspondence and offprint requests to: L. Pelletier, INSERM U28, Hopital Broussais, 96 rue Didot, 75674 Paris CEDEX 14, France

In Brown-Norway rats HgCl2 induces an autoimmune disease due to a T-dependent B cell polyclonal activation. This disease is marked by the production of numerous antibodies including antiglom-erular basement membrane (GBM) antibodies. Rats exhibit a biphasic glomerulopathy with heavy pro-teinuria. Initially anti-GBM antibodies are found linearly deposited; they precede the appearance of membranous glomerulopathy. Rats recover spontaneously even if HgCl2 injections are pursued, but mechanisms at play are unclear. We have assessed the effects of transplanting the spleen from a BN rat, either at the acme of the disease or at the time of convalescence, into naive BN rats, some of which were then injected with HgCl2- Transplantation of a spleen from HgCl2-injected rats at the acme of the disease dramatically protects BN rats from all the manifestations of the mercury disease. BN rats transplanted with a spleen from HgCl2-injected rats at the time of convalescence only exhibited a typical membranous glomerulopathy with heavy proteinuria but without circulating anti-GBM antibodies. Antilaminin antibodies were eluted from the glomeruli. This study shows that spleen cells from HgCl2-injected rats are able to confer tolerance to HgCl2-induced autoimmunity. It also shows that some B cell clones escape this tolerance. Finally, this study strongly suggests that membranous glomerulopathy, responsible for proteinuria in this model, is related to the presence of antilaminin antibodies.

Keywords: Antiglomerular basement membrane autoantibodies; Brown-Norway rat; HgCl2; membranous glomerulopathy; spleen transplantation; spontaneous regulation of autoimmunity


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