University of Amsterdam.
Blood. 2013 Aug 1;122(5):624-5. doi: 10.1182/blood-2013-06-508531.
In this issue of Blood, Moxon et al provide novel insight into the pathogenesis of cerebral malaria, linking loss of the endothelial protein C receptor (EPCR) on brain vessels, caused by cytoadherent infected erythrocytes, with localized coagulation, inflammation, and disruption of endothelial barrier function.
在本期《Blood》杂志中,Moxon 等人提供了关于脑型疟疾发病机制的新见解,将血管内皮蛋白 C 受体(EPCR)的缺失与局灶性凝血、炎症和内皮屏障功能障碍联系起来,而这种缺失是由黏附在血管上的被感染红细胞引起的。