Abstract. The pathogenesis of gold-induced autoimmu-nity and membranous glomerulopathy is not well under-stood. HgCl2 and D-penicillamine, other chemicals known to trigger membranous glomerulopathy in humans, induce autoimmune manifestations in Brown-Norway (BN) rats but not in Lewis (LEW) rats. These chemicals trigger T-cell clones which are specific for self class II molecules from the major histocompatibility complex and are probably responsible for the polyclonal B-cell activation observed. The aim of this work was to test the effects of aurothiopropanolsulphonate (ATPS) in BN and LEW rats. In BN rats, ATPS induced a polyclonal B-cell activation marked by lymphoproliferation, hyperimmu-noglobulinaemia affecting mainly IgE, and by the pro-duction of numerous autoantibodies. A glomeruloneph-ritis occurred, initially due to anti-glomerular basement membrane antibody deposition, and later to the form-ation of granular deposits, occasionally resulting in a typical membranous glomerulopathy. Self class-II-specific T-cells were found that might be responsible for the polyclonal B-cell activation. Lewis rats were free of glomerulopathy but, like BN rats, exhibited an intersti-tial nephritis and some degree of polyclonal B-cell activation. These findings demonstrate that, depending on the strain, ATPS triggers different B-cell clones inducing different degrees of autoimmunity
To submit an update or takedown request for this paper, please submit an Update/Correction/Removal Request.