Biggs B A, Goozé L, Wycherley K, Wilkinson D, Boyd A W, Forsyth K P, Edelman L, Brown G V, Leech J H
Walter and Eliza Hall Institute of Medical Research, Melbourne, Victoria, Australia.
J Exp Med. 1990 Jun 1;171(6):1883-92. doi: 10.1084/jem.171.6.1883.
The survival of Plasmodium falciparum-infected erythrocytes is enhanced by the sequestration of mature trophozoites and schizonts from the peripheral circulation. Cytoadherence of infected erythrocytes in vivo is associated with the presence of knobs on the erythrocyte surface, but we and others have shown recently that cytoadherence to C32 melanoma cells may occur in vitro in the absence of knobs. We show here that a knobless clone of P. falciparum adheres to the leukocyte differentiation antigen, CD36, suggesting that binding to CD36 is independent of the presence of knobs on the surface of the infected erythrocyte. This clone showed little cytoadherence to immobilized thrombospondin or to endothelial cells expressing the intercellular adhesion molecule 1. Furthermore, an Mr approximately 300-kD trypsin-sensitive protein doublet was immunoprecipitated from knobless trophozoite-infected erythrocytes. Finding a P. falciparum erythrocyte membrane protein 1 (PfEMP1)-like molecule on these infected erythrocytes is consistent with a role for PfEMP1 in cytoadherence to CD36 and C32 melanoma cells.
恶性疟原虫感染的红细胞通过将成熟滋养体和裂殖体与外周循环隔离而得以存活增强。体内受感染红细胞的细胞黏附与红细胞表面的凸起物有关,但我们和其他人最近表明,在体外没有凸起物的情况下,受感染红细胞也可能发生对C32黑色素瘤细胞的细胞黏附。我们在此表明,恶性疟原虫的一个无凸起克隆株可黏附于白细胞分化抗原CD36,这表明与CD36的结合不依赖于受感染红细胞表面凸起物的存在。该克隆株对固定化的血小板反应蛋白或对表达细胞间黏附分子1的内皮细胞几乎没有细胞黏附。此外,从无凸起滋养体感染的红细胞中免疫沉淀出一种分子量约为300 kD的胰蛋白酶敏感蛋白双联体。在这些受感染红细胞上发现类似恶性疟原虫红细胞膜蛋白1(PfEMP1)的分子,这与PfEMP1在对CD36和C32黑色素瘤细胞的细胞黏附中所起的作用是一致的。