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利用高度热标记抗原对兔实验性免疫复合物肾小球肾炎进行抗原特异性抑制。

Antigen-specific suppression of the experimental immune complex glomerulonephritis in rabbits by means of highly hot labelled antigen.

作者信息

Filipp G, Schumacher H, Dienes H P, Thoenes W, Biro G, Baumann B

出版信息

Allergol Immunopathol (Madr). 1984 Jul-Aug;12(4):251-7.

PMID:6209971
Abstract

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.

摘要

在一种新的实验模型中,即免疫复合物肾小球肾炎模型中,我们成功地几乎完全抑制了肾小球免疫疾病的发展。预先注射高度热标记的牛血清白蛋白(BSA)能够非常显著地预防肾损伤的出现。这一结果必须被解释为通过先前应用的高度热标记的BSA抑制抗BSA抗体合成的结果。由于缺乏抗BSA抗体,就不会形成抗原-抗体复合物,这些复合物不会沉积在肾小球基底膜中,肾小球免疫复合物疾病也不会发展。仅放射性(与人生长激素(HGH)偶联的125I)无法改变或抑制抗体的合成,因此也无法抑制抗原-抗体复合物的形成。

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Antibody affinity and acute immune complex disease.
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