Baruch D I, Pasloske B L, Singh H B, Bi X, Ma X C, Feldman M, Taraschi T F, Howard R J
Affymax Research Institute Santa Clara, California 95051, USA.
Cell. 1995 Jul 14;82(1):77-87. doi: 10.1016/0092-8674(95)90054-3.
Plasmodium falciparum-infected human erythrocytes evade host immunity by expression of a cell-surface variant antigen and receptors for adherence to endothelial cells. These properties have been ascribed to P. falciparum erythrocyte membrane protein 1 (PfEMP1), an antigenically diverse malarial protein of 200-350 kDa on the surface of parasitized erythrocytes (PEs). We describe the cloning of two related PfEMP1 genes from the Malayan Camp (MC) parasite strain. Antibodies generated against recombinant protein fragments of the genes were specific for MC strain PfEMP1 protein. These antibodies reacted only with the surface of MC strain PEs and blocked adherence of these cells to CD36 but without effect on adherence to thrombospondin. Multiple forms of the PfEMP1 gene are apparent in MC parasites. The molecular basis for antigenic variation in malaria and adherence of infected erythrocytes to host cells can now be pursued.
恶性疟原虫感染的人类红细胞通过表达细胞表面变异抗原和内皮细胞黏附受体来逃避宿主免疫。这些特性归因于恶性疟原虫红细胞膜蛋白1(PfEMP1),它是寄生红细胞(PEs)表面一种抗原性多样的200 - 350 kDa的疟疾蛋白。我们描述了从马来亚营地(MC)寄生虫株克隆两个相关的PfEMP1基因。针对这些基因的重组蛋白片段产生的抗体对MC株PfEMP1蛋白具有特异性。这些抗体仅与MC株PEs的表面发生反应,并阻断这些细胞与CD36的黏附,但对与血小板反应蛋白的黏附没有影响。PfEMP1基因的多种形式在MC寄生虫中很明显。现在可以探究疟疾抗原变异以及感染红细胞与宿主细胞黏附的分子基础了。