Hapten-specific cellular immune response producing glomerular injury.
A new model of experimental glomerulonephritis (GN) in which a cell-mediated (delayed-type) reaction predominated was established. Cationized TNP-BSA conjugates were planted in the kidney of rats by perfusion via the renal artery. Rats which had been sensitized with the TNP hapten 7 days previously revealed marked exudative and proliferative changes in their glomeruli, accompanied by transient proteinuria. A cellular influx was seen without deposition of any autologous antibody. The resulting data are compatible with the idea that cell-mediated immune reactions can participate in tissue damage in glomerular disease.
Oite
T
T
Department of Immunology, Niigata University School of Medicine, Japan.
Shimizu
F
F
Kagami
S
S
Morioka
T
T
D000818:Animals; D000917:Antibody Formation; D003877:Dermatitis, Contact / Q000276:immunology; D000939:Epitopes / Q000276:immunology*; D005921:Glomerulonephritis / Q000209:etiology / Q000276:immunology* / Q000473:pathology; D006241:Haptens / Q000276:immunology*; D006968:Hypersensitivity, Delayed / Q000276:immunology*; D008297:Male; D011507:Proteinuria / Q000209:etiology; D051381:Rats; D011919:Rats, Inbred Strains; D012710:Serum Albumin, Bovine / Q000276:immunology* / Q000493:pharmacokinetics; D014301:Trinitrobenzenes / Q000276:immunology
D000939:Epitopes; D006241:Haptens; D014301:Trinitrobenzenes; C038601:trinitrophenyl-bovine serum albumin; D012710:Serum Albumin, Bovine