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脑型疟疾(CM)是人恶性疟原虫感染最为严重并危及生命的疾病之一。以前主要依赖于组织学和生理学方法来推测其发病机理,并提出了不少假说,近年来应用动物模型和分子生物学技术,从分子水平加以研究,取得了很大进展。本文着重介绍分子水平的疟原虫寄生红细胞(PRBC)和宿主内皮细胞(EC)之间相互作用机制。 PRBC与EC间粘附导致血流阻滞并引起病理变化是疟原虫与宿主免疫系统间相互作用的复杂过程。很多因素影响着疟原虫寄生红细胞在体内粘附滞留部位及脑病变程度。针对EC的PRBC特异性受体表型不
Cerebral malaria (CM) is one of the most serious and life-threatening diseases in human P. falciparum. Previously relied mainly on histological and physiological methods to speculate on the pathogenesis and put forward many hypotheses. In recent years, the application of animal models and molecular biology techniques, from the molecular level to be studied, made great progress. This article focuses on the molecular mechanisms of the interaction between parasitic erythrocytes (PRBCs) and host endothelial cells (ECs). Adhesion between PRBC and EC leads to blockade of blood flow and cause pathological changes, which is a complex process of the interaction between the immune system of the host and the parasite. Many factors affect the malaria parasitic red blood cells in the body adhesion retention sites and brain lesions. The PRBC-specific receptor phenotype against EC is not