CYTOADHERENCE OF KNOBLESS PLASMODIUM-FALCIPARUM-INFECTED ERYTHROCYTES AND ITS INHIBITION BY A HUMAN MONOCLONAL-ANTIBODY
CYTOADHERENCE OF KNOBLESS PLASMODIUM-FALCIPARUM-INFECTED ERYTHROCYTES AND ITS INHIBITION BY A HUMAN MONOCLONAL-ANTIBODY
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DOI：
10.1038/338763a0
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发表时间：
1989-04-27
期刊：
影响因子：
64.8
通讯作者：
PERLMANN, P
中科院分区：
文献类型：
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作者：
UDOMSANGPETCH, R;AIKAWA, M;PERLMANN, P
感染了成熟期恶性疟原虫的红细胞与毛细血管和小静脉的内皮细胞结合。这种隔离对寄生虫的生存很重要，但可能对宿主产生严重后果。例如，它与导致25%死亡率的脑型疟疾的病因有关1 -5。受感染红细胞表面存在的旋钮状突起被认为是这种细胞粘附所必需的，但还不足以实现这种细胞粘附6 -8。在这里，我们描述了粘附到内皮细胞的感染的红细胞没有旋钮。一种人单克隆抗体（33 G2），它对一种表位具有特异性，该表位含有在某些确定的P的重复氨基酸序列中存在的规则间隔的谷氨酸二聚体。发现恶性疟原虫抗原9，10抑制细胞粘附，因此可能是阐明寄生虫隔离的分子基础的重要试剂。
RED blood cells infected with mature stages of the malaria parasitePlasmodium falciparumbind to the endothelial lining of capillaries and venules. This sequestration is important for the survival of the parasite but may have severe consequences for the host. For example, it is involved in the causation of cerebral malaria which carries 25% mortality1–5. Knob-like protrusions present on the surface of infected erythrocytes have been considered necessary but not sufficient for this cytoadherence6–8. Here we describe the adhesion to endothelial cells of infected erythrocytes which do not have knobs. A human monoclonal antibody (33G2) which was specific for an epitope containing regularly spaced dimers of glutamic acid present in the repeated amino-acid sequences of some definedP. falciparum antigens9,10was found to inhibit cytoadherence and may therefore be an important reagent for elucidating the molecular basis of parasite sequestration.