Jenkins C S, Ali-Briggs E F, Clemetson K J
Br J Haematol. 1981 Nov;49(3):439-47. doi: 10.1111/j.1365-2141.1981.tb07247.x.
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.
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。