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Isologous monoclonal antibodies can induce anti‐GBM glomerulonephritis in rats
Author(s) -
Sado Yoshikazu,
Kagawa Megumi,
Rauf Syarifuddin,
Naito Ichiro,
Moritoh Chiharu,
Okigaki Tohru
Publication year - 1992
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/path.1711680211
Subject(s) - nephritis , monoclonal antibody , glomerulonephritis , antibody , glomerular basement membrane , basement membrane , subclass , kidney , monoclonal , spleen , proteinuria , immunology , pathology , microbiology and biotechnology , biology , medicine
Injection of isologous monoclonal antibodies (SR2, SR3) caused anti‐glomerular basement membrane antibody‐induced glomerulonephritis (anti‐GBM nephritis) in WKY/NCrj rats. The antibodies were obtained from hybridoma cells derived from fusion of the spleen of a nephritic WKY/NCrj ral injected with rat solubilized renal basement membranes with adjuvant, and mouse SP2 myeloma cells. They belonged to the rat IgG2a subclass and bound to rat kidney in a linear pattern along the glomerular and tubular basement membranes. Histological changes in glomeruli were detected at day 1 after the injection; proteinuria with haematuria appeared on day 2; and proteinuria became severe and reached a plateau by day 5. These results demonstrate that anti‐GBM nephritis can even be induced by an isologous monoclonal antibody and that the rat IgG2a subclass is at least nephritogenic. The experimental model of anti‐GBM nephritis with isologous monoclonal antibodies makes it possible and easier to analyse further the mechanism of anti‐GBM nephritis.