GBM antigen prepared from four models of experimental GN [Masugi nephritis (rabbit anti-rat GBM antibody induced GN), passive Heymann nephritis, autologous immune complex nephritis, chronic serum sickness (BSA) nephritis] and normal rats were used in this study. The rats were immunized with the GBM antigen isolated from kidneys of various expe-rimental GN rats and complete Freund's adjuvant once a week for five times. All rats were sacrificed 35 to 60 days after first immunization. All of the experimental rats which were immunized with GBM antigen derived from Masugi nephritis demonstrated proliferative GN associated with crescent formation in 40% and tubulointerstitial nephritis in 30%. By immunofluorescence (IF), the kidney showed li-near deposits of rat IgG along the GBM in 100% and the tubular basement membrane (TBM) in 30%, whereas staining for rabbit IgG was consistently negative. By indirect IF, linear staining for rat IgG in the eluate from kidney of the same group was seen along GBM and TBM in the kidney of normal Wistar rats, mice, rabbits, but only along GBM in the kidney of human and guinea pigs. And the antibody was found to have no reactivity of BM of other organs such as liver, lung and spleen. In the experiments of passive transfer by means of the injection with the eluate obtai-ned from the kidney of the same group, continuous linear deposits of rat IgG were seen along GBM in recepient rats. The kidney sections of rats immunized with GBM from the other experimental GN rats ?and from normal rats demonstrated no abnormalities by light microscopy and IF. These results suggested that the immunization with GBM antigens derived from the kidney of Masugi nephritis elicited autoantibody against GBM and induced autoimmune anti-GBM antibody mediated GN. Moreover, we could demonstrate that the anti-GBM autoantibody seemed to have a nature of kidney specificity and a reactivity with both GBM and TBM in rats, mice and rabbits and only with GBM in human and guinea pigs.