In situ
immune complex glomerulonephritis can be induced in the rat employing cationized
antigen planted in the glomerular basement membrane (GBM) as a target for specific antibody. Another possible mechanism of in situ
immune complex formation is antibody already present in the GBM to bind circulating
antigen. Present study was performed in order to determine whether cationized
antibodies planted in the GBM could react with anionic as well as cationic
antigens to form immune deposits. Horse
ferritin, rabbit antibody to horse native
ferritin (f-Ab) and rabbit antibody to
ovalbumin (o-Ab) were highly cationized as described by Danon et al. The ability of the cationized
antibodies to precipitate
antigens was estimated by Ouchterlony analysis. 500 micrograms/100 g
body weight (b.w.) of cationized f-Ab or o-Ab was perfused into the left renal artery of male Wistar rats and 0.1-10.0 mg/100 g b.w. of either native or
cationized ferritin or
ovalbumin was injected respectively into the tail vein 1 hr later. Estimation of
proteinuria was done and the kidneys were removed up to 5 days for immunohistological as well as electron microscopical examination. Cationized
antibodies bound to anionic sites of the GBM and combined with subsequently injected
cationized ferritin or native
ovalbumin in situ, both leading to formation of subepithelial immune deposit with activation of C3 and caused mild
proteinuria. Native
ferritin, however, induced neither subepithelial immune deposit nor
proteinuria, because it didn't permeate through the GBM. The presented model indicates that antibody molecules of high positive charge can bind to the GBM and react with specific
antigens that are traversing the barrier to form immune deposits. This is independent of the charge of
antigen provided that the
antigen molecules are permeable into the GBM, as is the case with
ovalbumin but not native
ferritin.