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[Erythrocytes infected by Plasmodium falciparum activate human platelets].被恶性疟原虫感染的红细胞激活人类血小板。
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Platelets beyond their count, as a key element of the innate immune system in the fight against malaria.血小板数量之外，作为对抗疟疾的先天免疫系统的关键要素。
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本文引用的文献

1
Platelet factor 4 activity against P. falciparum and its translation to nonpeptidic mimics as antimalarials.血小板因子 4 对疟原虫的活性及其作为抗疟药的非肽模拟物的转化。
Cell Host Microbe. 2012 Dec 13;12(6):815-23. doi: 10.1016/j.chom.2012.10.017.
2
Platelet factor 4 and Duffy antigen required for platelet killing of Plasmodium falciparum.血小板因子 4 和达菲抗原是消灭恶性疟原虫所必需的。
Science. 2012 Dec 7;338(6112):1348-51. doi: 10.1126/science.1228892.
3
A phase 3 trial of RTS,S/AS01 malaria vaccine in African infants.RTS,S/AS01 疟疾疫苗在非洲婴儿中的 3 期临床试验。
N Engl J Med. 2012 Dec 13;367(24):2284-95. doi: 10.1056/NEJMoa1208394. Epub 2012 Nov 9.
4
Antipyretic measures for treating fever in malaria.治疗疟疾发热的退热措施。
Cochrane Database Syst Rev. 2012 Sep 12;2012(9):CD002151. doi: 10.1002/14651858.CD002151.pub2.
5
A long neglected world malaria map: Plasmodium vivax endemicity in 2010.一个长期被忽视的世界疟疾地图：2010 年间日疟原虫的流行情况。
PLoS Negl Trop Dis. 2012;6(9):e1814. doi: 10.1371/journal.pntd.0001814. Epub 2012 Sep 6.
6
Cerebral malaria pathogenesis: revisiting parasite and host contributions.脑型疟疾发病机制：重新审视寄生虫和宿主的作用。
Future Microbiol. 2012 Feb;7(2):291-302. doi: 10.2217/fmb.11.155.
7
Duffy negative antigen is no longer a barrier to Plasmodium vivax--molecular evidences from the African West Coast (Angola and Equatorial Guinea).达菲阴性抗原不再是阻碍间日疟原虫传播的障碍——来自非洲西海岸（安哥拉和赤道几内亚）的分子证据。
PLoS Negl Trop Dis. 2011 Jun;5(6):e1192. doi: 10.1371/journal.pntd.0001192. Epub 2011 Jun 21.
8
The global distribution of the Duffy blood group.杜菲血型的全球分布。
Nat Commun. 2011;2:266. doi: 10.1038/ncomms1265.
9
A plethora of Plasmodium species in wild apes: a source of human infection?野生猿类中存在大量疟原虫物种：人类感染的源头？
Trends Parasitol. 2011 May;27(5):222-9. doi: 10.1016/j.pt.2011.01.006. Epub 2011 Feb 25.
10
Origin of the human malaria parasite Plasmodium falciparum in gorillas.人类疟原虫恶性疟原虫起源于大猩猩。
Nature. 2010 Sep 23;467(7314):420-5. doi: 10.1038/nature09442.

对血小板在疟疾感染中保护作用的新见解。

New insights into the protective power of platelets in malaria infection.

作者信息

McMorran Brendan J, Burgio Gaetan, Foote Simon J

机构信息

Australian School of Advanced Medicine; Macquarie University; Macquarie Park, NSW Australia.

出版信息

Commun Integr Biol. 2013 May 1;6(3):e23653. doi: 10.4161/cib.23653.

DOI:10.4161/cib.23653
PMID:23710276
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3656011/
Abstract

Platelets, as well as regulating blood hemostasis, are an important component of the body's defense against invading microbial pathogens. We previously reported that platelets protect during malaria infection by binding Plasmodium-infected erythrocytes (IE) and killing the parasite within. More recent studies have now revealed the platelet plasmocidal factor, platelet factor 4 (PF4) and the red cell-expressed Duffy-antigen molecule as the central players in the parasite killing activity of platelets.

摘要

血小板除了调节血液止血外，还是机体抵御入侵微生物病原体防御系统的重要组成部分。我们之前报道过，血小板在疟疾感染期间通过结合疟原虫感染的红细胞（IE）并杀死其中的寄生虫来发挥保护作用。最近的研究现已揭示，血小板杀菌因子、血小板因子4（PF4）以及红细胞表达的达菲抗原分子是血小板杀灭寄生虫活性的核心参与者。