Smith H, Nelson J A, Gahmberg C G, Crandall I, Sherman I W
Department of Biology, University of California, Riverside 92521.
Exp Parasitol. 1992 Nov;75(3):269-80. doi: 10.1016/0014-4894(92)90212-s.
The cytoadherence of Plasmodium falciparum-infected erythrocytes (FCR-3 line) to human brain capillary endothelial cells (HBEC), C32 amelanotic melanoma cells, and human umbilical vein endothelial cells (HUVEC) was studied. The adhesion of infected red cells was HBEC > amelanotic melanoma > HUVEC. The presence or absence of the adhesive ligands ICAM-1 (CD54 or intercellular adhesion molecule 1), ICAM-2, and CD36 (= glycoprotein IV) was determined for each of these cells by indirect immunofluorescence using the monoclonal antibodies RR1/1, 6D5, and OKM 5/OKM 8, respectively. It appeared that a major ligand for the FCR-3 line of P. falciparum with amelanotic melanoma cells and HBECs was CD36. Binding to HUVECs was very low, presumably due to their lack of expression of CD36. HBECs, because of their ease of in vitro propagation, long-term maintenance of cytoadherent properties, and their high degree of adhesiveness, will be useful for in vitro studies of adherence.
研究了恶性疟原虫感染的红细胞(FCR-3株)与人脑微血管内皮细胞(HBEC)、C32无黑色素黑色素瘤细胞和人脐静脉内皮细胞(HUVEC)的细胞黏附情况。感染红细胞的黏附能力为HBEC>无黑色素黑色素瘤细胞>HUVEC。分别使用单克隆抗体RR1/1、6D5和OKM 5/OKM 8,通过间接免疫荧光法测定了这些细胞中黏附配体细胞间黏附分子-1(ICAM-1,即CD54)、ICAM-2和CD36(即糖蛋白IV)的有无。结果显示,恶性疟原虫FCR-3株与无黑色素黑色素瘤细胞及HBEC的主要配体是CD36。与HUVEC的结合非常低,推测是由于它们缺乏CD36的表达。HBEC因其易于体外培养、能长期维持细胞黏附特性且黏附性高,将有助于黏附的体外研究。