【摘要】 受恶性疟原虫感染的宿主红细胞会进行细胞重建,其中最明显的改变就是受染红细胞表面出现很多疣状突起(knob)。恶性疟红细胞膜相关蛋白1(PfEMP1)是疟原虫产生的毒性蛋白;这种蛋白通过受染红细胞表面的疣状突起被锚定在红细胞表面,介导红细胞与宿主内皮细胞受体结合,从而使恶性疟原虫能够逃避宿主的清除,并因阻塞作用致宿主脏器功能受损。PfEMP1由疟原虫基因组编码产生,通过其自身的一些特殊结构域将PfEMP1输送至包绕恶性疟原虫的纳虫空泡。由于红细胞没有亚细胞器,因此疟原虫必须建立自己的蛋白运输通路方可将虫体蛋白运至宿主细胞表面。受染红细胞胞质出现的茂氏裂褶是一种分泌细胞器,它将毒性蛋白由纳虫空泡运至红细胞膜表面。更多还原

【Abstract】 One of the obvious modifications of Plasmodium falciparum-infected erythrocytes is the development of thousands of knobs.The virulence protein,P.falciparum erythrocyte membrane protein 1(PfEMP1),is anchored on the outer face of erythrocytes via the knobs and mediates the adhesion of infected erythrocytes to the endothelial cells,thereby avoiding splenic clearance and resulting in host organ dysfunction due to the accumulation of infected erythrocytes within microvasculature.The PfEMP1 expressed by the parasite’s genome is exported to the parasitophorous vacuole in accordance with the specific domains of the protein.Since mature erythrocytes lack subcelluar organelles,the transportation of parasite proteins to the outside of the host cell depends on the parasite’s protein trafficking.Maurer’s clefts are secretory organelles that play an important role in the export of PfEMP1 from PV to the host cytosol and membrane.更多还原