Ockenhouse C F, Ho M, Tandon N N, Van Seventer G A, Shaw S, White N J, Jamieson G A, Chulay J D, Webster H K
Department of Medicine, Walter Reed Army Medical Center, Washington, DC.
J Infect Dis. 1991 Jul;164(1):163-9. doi: 10.1093/infdis/164.1.163.
The CD36 and ICAM-1 glycoproteins on vascular endothelial cells have been implicated as cytoadherence receptors for Plasmodium falciparum-infected erythrocytes (IRBC). Adhesion of IRBC from Thai patients with uncomplicated and severe falciparum malaria to purified CD36 or ICAM-1 and to C32 melanoma cells was compared. All malaria isolates bound to solid phase-adsorbed CD36 and to fluid-phase 125I-labeled CD36. IRBC adhesion to purified ICAM-1 varied widely, and no correlation with clinical severity of disease was observed. The cytoadherent phenotype of IRBC was modulated by selective panning on plates coated with purified CD36 or ICAM-1. IRBC selected by panning on CD36+, ICAM-1+ melanoma cells bound to cells that express surface CD36 but not to CD36-deficient cells, indicating that CD36 exerts a strong selective pressure on the IRBC cytoadherent phenotype. IRBC adhesion to CD36 and ICAM-1 suggests that P. falciparum parasites may use these receptors in vivo to promote parasite survival and immune evasion.
血管内皮细胞上的CD36和ICAM-1糖蛋白被认为是恶性疟原虫感染红细胞（IRBC）的细胞黏附受体。比较了来自泰国非复杂性和重症恶性疟患者的IRBC与纯化的CD36或ICAM-1以及C32黑色素瘤细胞的黏附情况。所有疟疾分离株均与固相吸附的CD36以及液相125I标记的CD36结合。IRBC对纯化的ICAM-1的黏附差异很大，且未观察到与疾病临床严重程度相关。IRBC的细胞黏附表型通过在包被有纯化的CD36或ICAM-1的平板上进行选择性淘选来调节。通过在CD36+、ICAM-1+黑色素瘤细胞上淘选而选择的IRBC与表达表面CD36的细胞结合，但不与缺乏CD36的细胞结合，这表明CD36对IRBC细胞黏附表型施加了强大的选择压力。IRBC对CD36和ICAM-1的黏附表明，恶性疟原虫寄生虫可能在体内利用这些受体来促进寄生虫存活和免疫逃避。
