CD36和细胞间黏附分子1介导恶性疟原虫发育中配子体的黏附。
CD36 and intercellular adhesion molecule 1 mediate adhesion of developing Plasmodium falciparum gametocytes.
作者信息
Rogers N J, Daramola O, Targett G A, Hall B S
机构信息
Department of Medical Parasitology, London School of Hygiene and Tropical Medicine, United Kingdom.
出版信息
Infect Immun. 1996 Apr;64(4):1480-3. doi: 10.1128/iai.64.4.1480-1483.1996.
Abstract
Plasmodium falciparum trophozoite-infected erythrocytes adhere to the amelanotic melanoma C32 cell line in vitro. Here we demonstrate for the first time that immature gametocyte-infected erythrocytes also adhere to C32 cells, albeit at lower levels than trophozoites. However, anti-CD36 and anti-intercellular adhesion molecule 1 antibodies inhibit asexual and gametocyte adhesion by comparable percentages, suggesting a common dependency for binding to these cellular receptors.
摘要
恶性疟原虫滋养体感染的红细胞在体外可黏附于无黑色素的黑色素瘤C32细胞系。在此，我们首次证明未成熟配子体感染的红细胞也能黏附于C32细胞，尽管其黏附水平低于滋养体。然而，抗CD36和抗细胞间黏附分子1抗体对无性生殖体和配子体黏附的抑制百分比相当，这表明二者在与这些细胞受体结合方面存在共同的依赖性。
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本文引用的文献
1
Sequestration in Plasmodium falciparum malaria: sticky cells and sticky problems.恶性疟原虫疟疾中的隔离：黏附细胞与棘手问题
Parasitol Today. 1990 Aug;6(8):247-54. doi: 10.1016/0169-4758(90)90184-6.
2
A strain theory of malaria transmission.疟疾传播的应变理论。
Parasitol Today. 1994 Dec;10(12):476-81. doi: 10.1016/0169-4758(94)90160-0.
3
Induction of adhesiveness in human endothelial cells by Plasmodium falciparum-infected erythrocytes.恶性疟原虫感染的红细胞对人内皮细胞黏附性的诱导作用。
Am J Trop Med Hyg. 1993 Apr;48(4):488-95. doi: 10.4269/ajtmh.1993.48.488.
4
Serological diversity of antigens expressed on the surface of erythrocytes infected with Plasmodium falciparum.恶性疟原虫感染的红细胞表面表达的抗原的血清学多样性。
Trans R Soc Trop Med Hyg. 1993 Sep-Oct;87(5):583-8. doi: 10.1016/0035-9203(93)90097-a.
5
Amplification of cytoadherence in cerebral malaria: towards a more rational explanation of disease pathophysiology.脑型疟疾中细胞黏附的增强：对疾病病理生理学更合理的解释
Ann Trop Med Parasitol. 1993 Dec;87(6):627-35. doi: 10.1080/00034983.1993.11812821.
6
An improved microassay for Plasmodium falciparum cytoadherence using stable transformants of Chinese hamster ovary cells expressing CD36 or intercellular adhesion molecule-1.一种利用表达CD36或细胞间黏附分子-1的中国仓鼠卵巢细胞稳定转化体改进的恶性疟原虫细胞黏附微量测定法。
Am J Trop Med Hyg. 1993 Mar;48(3):332-47. doi: 10.4269/ajtmh.1993.48.332.
7
The large diverse gene family var encodes proteins involved in cytoadherence and antigenic variation of Plasmodium falciparum-infected erythrocytes.庞大多样的var基因家族编码参与恶性疟原虫感染红细胞细胞黏附和抗原变异的蛋白质。
Cell. 1995 Jul 14;82(1):89-100. doi: 10.1016/0092-8674(95)90055-1.
8
Switches in expression of Plasmodium falciparum var genes correlate with changes in antigenic and cytoadherent phenotypes of infected erythrocytes.恶性疟原虫var基因表达的转换与受感染红细胞的抗原和细胞黏附表型的变化相关。
Cell. 1995 Jul 14;82(1):101-10. doi: 10.1016/0092-8674(95)90056-x.
9
Cloning the P. falciparum gene encoding PfEMP1, a malarial variant antigen and adherence receptor on the surface of parasitized human erythrocytes.克隆恶性疟原虫编码PfEMP1的基因，PfEMP1是一种疟疾变异抗原，也是被寄生的人类红细胞表面的黏附受体。
Cell. 1995 Jul 14;82(1):77-87. doi: 10.1016/0092-8674(95)90054-3.
10
Plasmodium falciparum: pfalhesin and CD36 form an adhesin/receptor pair that is responsible for the pH-dependent portion of cytoadherence/sequestration.恶性疟原虫：恶性疟原虫黏附素（pfalhesin）与CD36形成一个黏附素/受体对，该对负责细胞黏附/滞留的pH依赖性部分。
Exp Parasitol. 1994 Mar;78(2):203-9. doi: 10.1006/expr.1994.1020.
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