Passively transferred anti-brush border antibodies induce injury of proximal tubules in the absence of complement.
In active Heymann nephritis, antibodies directed against the brush border membrane of proximal tubules are able, when deposited in vivo, to cause substantial damage to the tubule epithelium. Prominent features of the lesion include fragmentation and loss of microvilli and proliferation of epithelial cells. Passive transfer of anti-brush border serum to appropriate proteinuric recipients also leads to proximal tubule pathology. In experiments reported here, full expression of the damage was observed in complement deficient recipients of passively transferred anti-brush border serum. A complement-independent process initiated by cross-linking of membrane determinants, which is analogous to the stimulation of B cell proliferation following cross-linking of Ig receptors by appropriate ligands, could account for the pathogenicity of anti-brush border serum.
D000818:Animals; D001323:Autoantibodies / Q000276:immunology*; D001327:Autoimmune Diseases / Q000276:immunology; D003165:Complement System Proteins / Q000172:deficiency*; D005260:Female; D007106:Immune Sera / Q000276:immunology; D007116:Immunization, Passive; D007136:Immunoglobulins / Q000032:analysis; D007687:Kidney Tubules, Proximal / Q000276:immunology* / Q000473:pathology; D008871:Microvilli / Q000276:immunology*; D009393:Nephritis / Q000276:immunology*; D051381:Rats; D011917:Rats, Inbred Lew
D001323:Autoantibodies; D007106:Immune Sera; D007136:Immunoglobulins; D003165:Complement System Proteins