Chulay J D, Ockenhouse C F
Walter Reed Army Institute of Research, Washington, DC.
Am J Trop Med Hyg. 1990 Aug;43(2 Pt 2):6-14. doi: 10.4269/ajtmh.1990.43.6.
Mature trophozoites and schizonts of Plasmodium falciparum induce changes in their host erythrocyte membranes that cause infected erythrocytes to sequester by binding to capillary endothelial cells. Sequestration protects infected erythrocytes from destruction in the spleen and contributes to the pathogenesis of severe and complicated malaria. The use of in vitro parasite culture and cytoadherence assays that measure the binding of infected erythrocytes to target cells has enabled the identification of host proteins that are putative receptors to which infected erythrocytes bind. Three such receptors have been identified: the extracellular matrix protein thrombospondin, the leukocyte differentiation antigen CD36, and the intercellular adhesion molecule ICAM-1. Infected erythrocytes can bind in vitro to each of these proteins. Thrombospondin and CD36 bind to one another, but each also binds to infected erythrocytes independently. Triggering of the CD36 receptor on platelets and monocytes activates these cells in vitro, and stimulation of endothelial cells with cytokines that upregulate ICAM-1 expression can increase the binding of infected erythrocytes to endothelial cells. Studies of these and perhaps other host receptors to which infected erythrocytes bind may contribute to our understanding of pathophysiologic mechanisms in malaria.
恶性疟原虫的成熟滋养体和裂殖体可诱导其宿主红细胞膜发生变化，导致受感染的红细胞通过与毛细血管内皮细胞结合而滞留。滞留可保护受感染的红细胞不被脾脏破坏，并促成严重和复杂疟疾的发病机制。利用体外寄生虫培养和细胞黏附试验来测量受感染红细胞与靶细胞的结合，已能够鉴定出作为受感染红细胞结合的假定受体的宿主蛋白。已鉴定出三种这样的受体：细胞外基质蛋白血小板反应蛋白、白细胞分化抗原CD36和细胞间黏附分子ICAM-1。受感染的红细胞在体外可与这些蛋白中的每一种结合。血小板反应蛋白和CD36相互结合，但它们也各自独立地与受感染的红细胞结合。血小板和单核细胞上CD36受体的激活在体外可激活这些细胞，用上调ICAM-1表达的细胞因子刺激内皮细胞可增加受感染红细胞与内皮细胞的结合。对这些以及可能其他受感染红细胞所结合的宿主受体的研究，可能有助于我们理解疟疾的病理生理机制。
