首页> 美国卫生研究院文献>The Journal of Clinical Investigation >Complement (C5-a)-induced granulocyte aggregation in vitro. A possible mechanism of complement-mediated leukostasis and leukopenia.
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Complement (C5-a)-induced granulocyte aggregation in vitro. A possible mechanism of complement-mediated leukostasis and leukopenia.

机译:补体(C5-a)诱导的粒细胞体外聚集。补体介导的白细胞减少和白细胞减少的可能机制。

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摘要

Activated plasma complement will induce biphasic aggregation of human granulocytes dectable by standard nephelometric techniques. The responsible active component was suggested to be C5a by molecular weight and heat-stability assays; moreover, aggragating activity was ablated by anti-C5 but not anti-C3 antibodies. C5a prepared by trypsinization of purified C5 reproduced the aggregating activity of whole activated plasma, whereas plasma from a C5-deficient donor did not support aggregation. Embolization of granulocyte aggregates might be a previously unsuspected cause of leukostasis and pulmonary damage in various clinical situations where intravascular complement activation occurs.
机译:活化的血浆补体将诱导人粒细胞的双相聚集,该粒细胞可通过标准浊度法测定。分子量和热稳定性分析表明,负责任的活性成分为C5a。此外,抗C5抗体消除了凝集活性,但抗C3抗体没有。通过胰蛋白酶消化纯化的C5制备的C5a再现了整个活化血浆的聚集活性,而来自C5缺陷供体的血浆则不支持聚集。在发生血管内补体激活的各种临床情况下,粒细胞聚集物的栓塞可能是白细胞停滞和肺部损伤的先前未曾预料的原因。

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