Rogers N J, Targett G A, Hall B S
Immunology and Cell Biology Unit, Department of Medical Parasitology, London School of Hygiene and Tropical Medicine, United Kingdom.
Infect Immun. 1996 Oct;64(10):4261-8. doi: 10.1128/iai.64.10.4261-4268.1996.
Plasmodium falciparum gametocyte-infected erythrocytes are characterized by their ability to sequester in the microvasculature of various organs, primarily the spleen and bone marrow. This phenomenon is thought to play a critical role in the development and survival of the sexual stages. Little is known, however, about ligands on the gametocyte-infected erythrocyte. Infection of erythrocytes with mature asexual stages of P. falciparum (trophozoites and schizonts) has been shown to induce modification of the erythrocyte anion transporter, band 3, and this has been linked to the acquisition of an adherent phenotype. Here, we demonstrate for the first time that immature gametocyte-infected erythrocytes also express modified band 3. In vitro binding assays demonstrate that gametocyte-infected erythrocytes of the 3D7 strain utilize this surface receptor for adhesion to C32 amelanotic melanoma cells via the host cell receptor CD36 (platelet glycoprotein IIIb). Adhesion of gametocyte-infected erythrocytes to CD36-transfected CHO cells is also dependent on modified band 3. However, modified band 3 does not mediate adhesion of gametocyte-infected erythrocytes to intercellular adhesion molecule 1, a second host receptor for gametocytes expressed on C32 cells.
恶性疟原虫配子体感染的红细胞的特征在于它们能够在各种器官的微脉管系统中滞留，主要是脾脏和骨髓。这种现象被认为在有性阶段的发育和存活中起关键作用。然而，关于配子体感染的红细胞上的配体却知之甚少。恶性疟原虫成熟无性阶段（滋养体和裂殖体）感染红细胞已被证明会诱导红细胞阴离子转运蛋白带3发生修饰，这与获得粘附表型有关。在此，我们首次证明未成熟配子体感染的红细胞也表达修饰的带3。体外结合试验表明，3D7株配子体感染的红细胞利用这种表面受体通过宿主细胞受体CD36（血小板糖蛋白IIIb）粘附于C32无黑色素黑色素瘤细胞。配子体感染的红细胞与CD36转染的CHO细胞的粘附也依赖于修饰的带3。然而，修饰的带3并不介导配子体感染的红细胞与细胞间粘附分子1的粘附，细胞间粘附分子1是C32细胞上表达的配子体的第二种宿主受体。
