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抗血小板膜糖蛋白抗体。II. 对二磷酸腺苷和胶原诱导的血小板聚集的影响、交叉免疫电泳研究及其与Glanzmann血小板无力症的相关性

Antibodies against platelet membrane glycoproteins. II. Influence on ADP- and collagen-induced platelet aggregation, crossed immunoelectrophoresis studies and relevance to Glanzmann's thrombasthenia.

作者信息

Jenkins C S, Ali-Briggs E F, Clemetson K J

出版信息

Br J Haematol. 1981 Nov;49(3):439-47. doi: 10.1111/j.1365-2141.1981.tb07247.x.

Abstract

In Glanzmann's thrombasthenia glycoproteins IIb and IIIa are missing or strongly reduced and aggregation to ADP, collagen and thrombin is impaired. Antibodies against glycoproteins IIb and IIIa did not entirely induce a thrombasthenia-like state in normal platelets. However, they did strongly inhibit collagen-induced aggregation and inhibited the second wave of aggregation induced by ADP. Crossed immunoelectrophoresis studies using Triton X-100 extracts of whole platelets with these antibodies gave a single immunoprecipitate. This immunoprecipitate was absent when similar studies were carried out with thrombasthenic platelets. Platelet antibodies gave a number of immunoprecipitates with normal platelets and differences were observed with thrombasthenic platelets, the most notable of which was a marked reduction in one of the major immunoprecipitates. These results provide further evidence that glycoproteins IIb and IIIa are involved in the latter stages of platelet aggregation.

摘要

在血小板无力症中,糖蛋白IIb和IIIa缺失或显著减少,对二磷酸腺苷(ADP)、胶原和凝血酶的聚集功能受损。针对糖蛋白IIb和IIIa的抗体并未在正常血小板中完全诱导出类似血小板无力症的状态。然而,它们确实强烈抑制胶原诱导的聚集,并抑制ADP诱导的第二波聚集。使用这些抗体对全血小板的Triton X - 100提取物进行交叉免疫电泳研究,得到单一免疫沉淀物。当对血小板无力症血小板进行类似研究时,这种免疫沉淀物不存在。血小板抗体与正常血小板产生了许多免疫沉淀物,并且在血小板无力症血小板中观察到差异,其中最显著的是主要免疫沉淀物之一明显减少。这些结果进一步证明糖蛋白IIb和IIIa参与血小板聚集的后期阶段。

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