Aotsuka S, Shibata S
Clinical Research Institute, National Medical Center, Tokyo, Japan.
Nephron. 1987;47(2):95-100. doi: 10.1159/000184468.
A single footpad injection of a triglycosyl glycopeptide (nephritogenoside, NG) isolated from rat glomerular basement membrane can induce proliferative glomerulonephritis (PGN) in homologous animals, resulting in contracted kidney. On the other hand, it is well known that administration of rat tubular brush border antigen (Fx1A) causes a membranous glomerulonephritis (MG) in homologous animals. When a partially purified NG (crude NG, cNG) is injected in rats, a mixed lesion of PGN and MG resulted. To investigate the correlation between renal glomerular lesions and humoral immune responses in animals given NG and cNG, levels of antibodies to cNG and Fx1A, and those of immune complexes (ICs) are measured in sera from animals of these experimental groups using enzyme-linked immunosorbent assay. Significant levels of antibodies to cNG and Fx1A and those of ICs are detected in all groups of rats injected with cNG, Fx1A and pronase-digested Fx1A. It was revealed that antibodies to cNG in sera from rats injected with cNG, Fx1A and pronase-digested Fx1A recognize the common epitopes shared with Fx1A. On the other hand, neither antibodies nor ICs are detected in rats injected with NG, suggesting that humoral immune mechanisms may not play a leading role in the pathogenesis of NG-induced glomerulonephritis.
