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无法用可溶性细胞间黏附分子-1（ICAM-1）阻断恶性疟原虫感染的红细胞与ICAM-1的黏附。

Failure to block adhesion of Plasmodium falciparum-infected erythrocytes to ICAM-1 with soluble ICAM-1.

作者信息

Craig A G, Pinches R, Khan S, Roberts D J, Turner G D, Newbold C I, Berendt A R

机构信息

Molecular Parasitology Group, Institute of Molecular Medicine, John Radcliffe Hospital, Oxford, United Kingdom.

出版信息

Infect Immun. 1997 Nov;65(11):4580-5. doi: 10.1128/iai.65.11.4580-4585.1997.

DOI:10.1128/iai.65.11.4580-4585.1997
PMID:9353036
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC175657/
Abstract

The adhesion of Plasmodium falciparum-infected erythrocytes is thought to play a central role in the pathogenesis of severe malaria. ICAM-1 has been identified as one of the host receptors for parasitized erythrocytes and has been implicated as being involved in progression to cerebral malaria. Thus, intervention strategies based on the reversal of this interaction could potentially be used to reduce morbidity and mortality. We have investigated the inhibition of the interaction between ICAM-1 and infected erythrocytes by using recombinant soluble ICAM-1 as competitor and find that we are unable to reduce adhesion to ICAM-1 in vitro.

摘要

恶性疟原虫感染的红细胞的黏附被认为在重症疟疾的发病机制中起核心作用。细胞间黏附分子-1（ICAM-1）已被确定为被寄生红细胞的宿主受体之一，并被认为与脑型疟疾的进展有关。因此，基于逆转这种相互作用的干预策略可能会被用于降低发病率和死亡率。我们使用重组可溶性ICAM-1作为竞争者，研究了对ICAM-1与感染红细胞之间相互作用的抑制作用，结果发现我们无法在体外降低对ICAM-1的黏附。

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Failure to block adhesion of Plasmodium falciparum-infected erythrocytes to ICAM-1 with soluble ICAM-1.无法用可溶性细胞间黏附分子-1（ICAM-1）阻断恶性疟原虫感染的红细胞与ICAM-1的黏附。
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Molecular cloning of a gene from Plasmodium falciparum that codes for a protein sharing motifs found in adhesive molecules from mammals and plasmodia.恶性疟原虫中一个基因的分子克隆，该基因编码一种蛋白质，其具有在哺乳动物和疟原虫的黏附分子中发现的共有基序。
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