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Research Article Free access | 10.1172/JCI113021

Glomerulonephritis induced in the rabbit by antiendothelial antibodies.

S Matsuo, A Fukatsu, M L Taub, P R Caldwell, J R Brentjens, and G Andres

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Published June 1, 1987 - More info

Published in Volume 79, Issue 6 on June 1, 1987
J Clin Invest. 1987;79(6):1798–1811. https://doi.org/10.1172/JCI113021.
© 1987 The American Society for Clinical Investigation
Published June 1, 1987 - Version history
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Abstract

The effects of interaction between endothelial angiotensin converting enzyme (ACE) and goat anti-rabbit ACE (GtARbACE) antibodies were studied in rabbit glomeruli. By immunofluorescence ACE was not detectable in normal glomeruli. However, when kidneys were perfused with GtARbACE antibodies glomerular bound IgG was seven times higher than that of non-immune IgG and granular deposits of goat IgG were found on the endothelium of glomeruli and arteries. Rabbits injected intravenous for 4 d with GtARbACE antibodies showed on day 1 granular deposits of goat IgG on the glomerular endothelium; from day 3 to 24 there was gradual development of subepithelial deposits of goat IgG, rabbit IgG and C3. When GtARbACE antibodies were similarly injected into proteinuric rabbits there was formation of subepithelial granular deposits of goat IgG and ACE. The results document that a glomerular endothelial antigen is redistributed in vivo by a specific ligand, an event associated with formation of immune deposits. Furthermore, if the glomerular permeability is artificially increased, immune complexes shed from nonglomerular endothelia into the circulation can contribute to form subepithelial immune deposits.

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