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恶性疟原虫成熟红细胞表面抗原对于结节或细胞黏附并非必需。

The mature erythrocyte surface antigen of Plasmodium falciparum is not required for knobs or cytoadherence.

作者信息

Petersen C, Nelson R, Magowan C, Wollish W, Jensen J, Leech J

机构信息

Medical Service, San Francisco General Hospital CA 94110.

出版信息

Mol Biochem Parasitol. 1989 Aug;36(1):61-5. doi: 10.1016/0166-6851(89)90200-4.

Abstract

Intraerythrocytic Plasmodium falciparum parasites at the trophozoite and schizont stages synthesize a greater than 200-kDa protein, the mature erythrocyte surface antigen (MESA), that is localized at the membrane of infected red blood cells and manifests size polymorphism and antigenic diversity among parasite isolates. Because MESA is localized in the host cell membrane, we examined parasites with differing knob and cytoadherence phenotypes to determine whether MESA expression correlated with knob formation and cytoadherence. A cloned line of P. falciparum that was cultured with repeated selection for the knobbed and cytoadherent phenotypes did not express MESA, due to at least partial deletion of the single-copy MESA gene. In contrast, parasites from the same clone that were cultured without this selection lost the knobbed and cytoadherent phenotypes, but continued to express MESA. These results indicate that MESA is apparently not required for differentiation and multiplication of erythrocyte stage P. falciparum parasites in vitro, or for knob formation and cytoadherence. We speculate that MESA may have a role in evasion of the host immune response by P. falciparum.

摘要

处于滋养体和裂殖体阶段的红细胞内恶性疟原虫寄生虫会合成一种大于200 kDa的蛋白质,即成熟红细胞表面抗原(MESA),该抗原定位于被感染红细胞的膜上,并且在寄生虫分离株之间表现出大小多态性和抗原多样性。由于MESA定位于宿主细胞膜中,我们检测了具有不同凸起和细胞黏附表型的寄生虫,以确定MESA表达是否与凸起形成和细胞黏附相关。一个经过反复选择具有凸起和细胞黏附表型培养的恶性疟原虫克隆系不表达MESA,这是由于单拷贝MESA基因至少部分缺失所致。相反,来自同一克隆的未经这种选择培养的寄生虫失去了凸起和细胞黏附表型,但继续表达MESA。这些结果表明,MESA显然不是体外红细胞期恶性疟原虫寄生虫分化和增殖所必需的,也不是凸起形成和细胞黏附所必需的。我们推测MESA可能在恶性疟原虫逃避宿主免疫反应中起作用。

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