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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。
Host erythrocytes infected with P. falciparum undergo cell reconstitution, with the most noticeable change being the appearance of many knobs on the surface of infected erythrocytes. Plasmodium falciparum erythrocyte membrane associated protein 1 (PfEMP1) is a toxic protein produced by Plasmodium; this protein is anchored on the surface of erythrocytes by verrucous protrusions on the surface of infected erythrocytes, mediating the binding of erythrocytes to the receptor of endothelial cells of the host such that Plasmodium falciparum can evade host clearance and impaired host organ function due to obstruction. PfEMP1 is encoded by the Plasmodium genome and delivers PfEMP1 through its own specific domains to the parasite vacuoles surrounding Plasmodium falciparum. Because erythrocytes do not have subcellular organelles, plasmodia must establish its own protein trafficking pathway to transport the worm proteins to the host cell surface. Mochizuki’s fissure, which occurs in the cytoplasm of infected erythrocytes, is a secretory organelle that conveys toxic proteins from the orbital vacuole to the surface of the erythrocyte membrane.