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血小板免疫复合物相互作用在川崎病发病机制中的作用

Platelet immune complex interaction in the pathogenesis of Kawasaki disease.

作者信息

Levin M, Holland P C, Novelli V

机构信息

Department of Immunology, Institute of Child Health, London.

出版信息

Prog Clin Biol Res. 1987;250:227-37.

PMID:3423040
Abstract

We have shown that the thrombocytosis which occurs in the 3rd and 4th week of Kawasaki disease is associated with the appearance in the circulation of platelet aggregating factors detected by the PAT test. These factors induce aggregation and serotonin release from normal platelets. The aggregation can be blocked by EDTA and Prostacyclin. The aggregating factor appears to be of high molecular weight, and its activity was lost following fractionation at low pH. The platelet aggregating activity was significantly associated with the presence of IgG immune complexes, and these features suggest that IgG immune complexes are responsible for the platelet aggregating activity.

摘要

我们已经表明,川崎病第3周和第4周出现的血小板增多症与血小板聚集试验(PAT试验)检测到的血小板聚集因子在循环中的出现有关。这些因子可诱导正常血小板聚集并释放5-羟色胺。这种聚集可被乙二胺四乙酸(EDTA)和前列环素阻断。聚集因子似乎是高分子量的,在低pH值下分级分离后其活性丧失。血小板聚集活性与IgG免疫复合物的存在显著相关,这些特征表明IgG免疫复合物是血小板聚集活性的原因。

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