Antigen-specific suppression of the experimental immune complex glomerulonephritis in rabbits by means of highly hot labelled antigen.
We succeeded in suppressing almost completely the development of glomerular immune disease in a new experimental model, i.e. in the model of immune complex glomerulonephritis. Previous injection of highly hot labelled BSA was able to prevent very significantly the appearance of kidney injury. This result must be interpreted as the consequence of suppression of the synthesis of anti-BSA-antibody by means of previously applied highly hot labelled BSA. As a consequence of the lack of anti-BSA-antibodies there is no formation of antigen-antibody complexes, no deposition of these complexes in the glomerulus basement membrane, and no development of glomerular immune complex disease. Radioactivity alone (125I coupled to HGH) was not capable of modifying or suppressing the synthesis of antibody and consequently, the formation of antigen-antibody complexes.
D000818:Animals; D000921:Antibody-Producing Cells / Q000276:immunology / Q000528:radiation effects*; D000941:Antigens / Q000008:administration & dosage; D000939:Epitopes; D005921:Glomerulonephritis / Q000276:immunology* / Q000517:prevention & control; D007105:Immune Complex Diseases / Q000276:immunology* / Q000517:prevention & control; D007165:Immunosuppression Therapy; D007457:Iodine Radioisotopes / Q000008:administration & dosage; D011817:Rabbits; D012710:Serum Albumin, Bovine / Q000008:administration & dosage
D000941:Antigens; D000939:Epitopes; D007457:Iodine Radioisotopes; D012710:Serum Albumin, Bovine