Plasmodium falciparum malaria. An amelanotic melanoma cell line bears receptors for the knob ligand on infected erythrocytes.
Plasmodium falciparum malaria. An amelanotic melanoma cell line bears receptors for the knob ligand on infected erythrocytes.
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恶性疟原虫疟疾。
DOI：
10.1172/jci110627
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发表时间：
1982
期刊：
影响因子：
--
通讯作者：
Miller,LH
中科院分区：
文献类型：
--
作者：
Schmidt,JA;Udeinya,IJ;Leech,JH;Hay,RJ;Aikawa,M;Barnwell,J;Green,I;Miller,LH
感染恶性滋养体疟原虫和分裂体的红细胞在外周循环中看不到，因为它们通过感染红细胞膜上的结节状结构附着在静脉内皮上。我们最近发现含有p的红细胞。恶性滋养体和分裂体同样通过旋钮附着在培养的人静脉内皮细胞上。为了寻找一种更实用的靶细胞来进行大规模的结合研究，以表征和分离旋钮配体，我们测试了各种正常细胞和连续细胞系的结合能力。falciparum-infected红细胞。在测试的18种细胞类型中，观察到受感染的红细胞与人类无色素黑色素瘤细胞系和羊膜上皮细胞以及人类主动脉和脐静脉内皮细胞结合。96-100%的无色素黑色素瘤细胞每个阳性细胞结合17±4（±1 SEM）个感染红细胞，而内皮细胞（4-59%）和羊膜上皮细胞（8-19%）能够分别结合12±5和4±1个感染红细胞。进一步的研究旨在比较其与无色素黑色素瘤细胞系和内皮细胞的结合机制，结果如下：首先，受感染的红细胞与这两种细胞类型的粘附是寄生虫阶段特异性的，因为只有含有晚期环状体、滋养体和分裂体的红细胞才能结合。含有早期环型的红细胞，在体内不附着于静脉内皮，不与两种细胞类型结合。第二，红细胞感染滋养体和分裂体。vivaxor是一种无节菌株。恶性疟原虫，这两种都在体内继续循环，不与任何一种靶细胞类型结合。第三，透射电镜显示，受感染的红细胞通过旋钮附着在无色素黑色素瘤细胞上。我们得出结论，培养的人内皮细胞和无色素黑色素瘤细胞系在其表面具有共同的决定因子，并且与这两种不同细胞类型的结合机制是相似的。在需要大量靶细胞的结合研究中，无色素黑色素瘤细胞系提供了内皮细胞的有用替代品。图片
Erythrocytes infected withPlasmodium falciparumtrophozoites and schizonts are not seen in the peripheral circulation because they attach to venular endothelium via knoblike structures on the infected erythrocyte membrane. We have recently shown that erythrocytes containingP. falciparumtrophozoites and schizonts likewise attach to cultured human venous endothelial cells via knobs. In search of a more practical target cell for large scale binding studies designed to characterize and isolate the knob ligand, we tested various normal cells and continuous cell lines for their ability to bindP. falciparum-infected erythrocytes. Of the 18 cell types tested, binding of infected erythrocytes was observed to a human amelanotic melanoma cell line and amnion epithelial cells as well as to human aortic and umbilical vein endothelial cells. 96-100% of amelanotic melanoma cells bound 17±4 (±1 SEM) infected erythrocytes per positive cell, whereas fewer endothelial cells (4-59%) and amnion epithelial cells (8-19%) were capable of binding 12±5 and 4±1 infected erythrocytes per positive cell, respectively. Further studies designed to compare the mechanism of binding to the amelanotic melanoma cell line and endothelial cells showed the following results. First, that adhesion of infected erythrocytes to these two cell types was parasite stage-specific in that only erythrocytes containing late ring forms, trophozoites, and schizonts bound. Erythrocytes containing early ring forms, which do not attach to venular endothelium in vivo, did not bind to either cell type. Second, erythrocytes infected with trophozoites and schizonts ofP. vivaxor a knobless strain ofP. falciparum, both of which continue to circulate in vivo, did not bind to either target cell type. Third, transmission electron microscopy showed that infected erythrocytes attached to the amelanotic melanoma cells via knobs. We conclude that cultured human endothelial cells and an amelanotic melanoma cell line share common determinants on their surface and that the mechanism of binding to these two different cell types is similar. The amelanotic melanoma cell line offers a useful substitute for endothelial cells in binding studies requiring large numbers of target cells.Images