[Fixation of renal tubules in vivo by microperfusion in light and electron microscopic studies].
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Biomedical subjects
Publications and source records attributed to W Thoenes.
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In a previous experiment we were able to induce in rabbits a state of specific tolerance against bovine serum albumin (BSA) by pretreatment with highly hot labelled BSA-125 I thus preventing immune complex glomerulonephritis. Despite successful suppression of antibody production, the question remained to be answered if this was due to an nonspecific effect of immunosuppression by radio-iodinated BSA or caused by the elimination of the corresponding lymphocyte clone according to the clonal deletion theory. Therefore, rabbits, rendered tolerant BSA antigen were treated with another antigen, bovine gamma globulin (BCG) and developed classical immune complex glomerulonephritis and vice versa. These results strongly suggest a specific elimination of the effector cell clones only, the exact mechanism of which still remains to be elucidated.
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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.