家兎抗刷子縁抗体による自己免疫Heymann腎炎の発症

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タイトル別名
  • Experimental autoimmune Heymann nephritis induced by immunization with rabbit anti-brush border antibody associated glomeruli.

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Three different types of glomeruli isolated from active Heymann nephritis (ANH) -, passive heymann nephritis (PHN) - and normal Wistar rat were used for induction of glomerulonepritis. These glomeruli were emulsified in Freund's complete adjuvant and were immunized to Wistar rats once a week for total of five to seven times. All rats were unilaterally nephrectomized at 35 day and sacrificed at 60 day after first immunization. The specimens of the kidneys were studied under light microscopy and immunofluorescene microscopy. By direct immunofluorescene study, the specimens from the rats which were immunized with PHN-glomeruli and were unilaterally nephectomized at 35 day revealed faint deposits of rat IgG in granular pattern along the glomerular capillary loops. The intensity of the deposits became more prominent at 60 day. During the time of observation, no deposits of rabbit IgG were found in the kidney of the experimental rats. Whereas the kidneys obtained from the rats which were immunized with AHN- or normal-glomeruli revealed no deposit in glomeruli at all. By light microscopy, the specimen from rats which were immunized with PHN-glomeruli showed slight thickening of capillary loop, but no proliferation of mesagial cells and no infiltration of inflamatory cells. The other groups of the experimental rat demonstrated no abnormal findings. By indirect immunofluorescence study using FITC labeled goat anti-rat IgG antibody, the eluate from the kidney which were immunized with PHN-glomeruli shows to have a reactivity with proximal tubular brush border. These results suggested that the immunization with glomerular antigen binding rabbit antirat brush border antibody elicited autoantibody against brush border and induced antibrush border autoantibody mediated glomerulo nephritis. From these results, we speculated that net work system, such as anti-anti brush border antibody and the anti-idiotypic antibody played an important role for induction of the autoantibody and of autologous immune complex glomerulonephritis.

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