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补体(C5-a)诱导的体外粒细胞聚集。补体介导的白细胞停滞和白细胞减少的一种可能机制。

Complement (C5-a)-induced granulocyte aggregation in vitro. A possible mechanism of complement-mediated leukostasis and leukopenia.

作者信息

Craddock P R, Hammerschmidt D, White J G, Dalmosso A P, Jacob H S

出版信息

J Clin Invest. 1977 Jul;60(1):260-4. doi: 10.1172/JCI108763.

DOI:10.1172/JCI108763
PMID:874088
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC372364/
Abstract

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.

摘要

活化的血浆补体可诱导人粒细胞发生双相聚集,这可通过标准比浊技术检测到。通过分子量和热稳定性分析表明,起作用的活性成分是C5a;此外,抗C5抗体可消除聚集活性,而抗C3抗体则不能。通过胰蛋白酶消化纯化的C5制备的C5a重现了全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,粒细胞聚集体的栓塞可能是白细胞淤滞和肺损伤的一个先前未被怀疑的原因。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1aac/372364/5444800b2729/jcinvest00655-0270-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1aac/372364/5444800b2729/jcinvest00655-0270-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1aac/372364/5444800b2729/jcinvest00655-0270-a.jpg

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