Lack of passive transfer of renal tubulointerstitial disease by serum or monoclonal antibody specific for renal tubular antigens in the mouse

• Published in: International archives of allergy and applied immunology Vol. 86; no. 2; p. 238
• Main Authors: Evans, B D, Dilwith, R L, Balaban, S L, Rudofsky, U H
• Format: Journal Article
• Language: English
• Published: Switzerland 1988
• Subjects: Animals; Antibodies, Monoclonal - administration & dosage; Antibody Specificity; Antigens - immunology; Autoantigens - immunology; Basement Membrane - immunology; Guinea Pigs; Immunization, Passive - methods; Kidney Glomerulus - immunology; Kidney Tubules - immunology; Mice; Mice, Inbred Strains; Nephritis, Interstitial - blood; Nephritis, Interstitial - immunology
• ISSN: 0020-5915
• DOI: 10.1159/000234578

Mice immunized with rabbit renal basement membranes form autoantibodies to their kidney glomerular and tubular basement membranes (GBM/TBM). Development of renal tubular disease (RTD) consists of deposition of autoantibodies along the GBM/TBM with the inter- and intratubular accumulation of lymphocytes and macrophages and destruction of the TBM. Transfer of this disease in mice with either serum or monoclonal antibodies, however, has been difficult to demonstrate and, therefore, attempts were made to confirm a report that RTD is passively transferred by anti-TBM autoantibodies. Using the revised protocol in this later report, we found that 12 weeks after transfer autoantibodies were deposited along the GBM and/or TBM of the recipients, yet RTD was not observed. Although qualitative and quantitative characteristics of the antibody may play a role in the pathogenesis in the murine model of RTD, we could not obtain evidence to support and confirm this study.