Plasmodium falciparum picks (on) EPCR

被引：31

作者：

Aird, William C. ^{[1
,2
]}

Mosnier, Laurent O. ^{[3
]}

Fairhurst, Rick M. ^{[4
]}

机构：

[1] Beth Israel Deaconess Med Ctr, Vasc Biol Res Ctr, Boston, MA 02215 USA

[2] Beth Israel Deaconess Med Ctr, Dept Med, Boston, MA 02215 USA

[3] Scripps Res Inst, Dept Mol & Expt Med, La Jolla, CA 92037 USA

[4] NIAID, Lab Malaria & Vector Res, NIH, Bethesda, MD 20892 USA

来源：

BLOOD | 2014年 / 123卷 / 02期

关键词：

PROTEIN-C RECEPTOR; DIFFERENTIAL REACTIVITY; CEREBRAL MALARIA; ANTICOAGULANT; BINDING; ENDOTHELIUM; COAGULATION; INSIGHTS; CELLS;

D O I：

10.1182/blood-2013-09-521005

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Of all the outcomes of Plasmodium falciparum infection, the coma of cerebral malaria (CM) is particularly deadly. Malariologists have long wondered how some patients develop this organ-specific syndrome. Data from two recent publications support a novel mechanism of CM pathogenesis in which infected erythrocytes (IEs) express specific virulence proteins that mediate IE binding to the endothelial protein C receptor (EPCR). Malaria-associated depletion of EPCR, with subsequent impairment of the protein C system promotes a proinflammatory, procoagulant state in brain microvessels.

引用

页码：163 / 167

页数：5

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