Facer C A
Trans R Soc Trop Med Hyg. 1983;77(4):524-30. doi: 10.1016/0035-9203(83)90130-x.
Human erythrocytes with a deficiency in glycophorin A (En(a-) cells) and glycophorin B (S-s-U- and S-s-U+ cells) show significant resistance in vitro to invasion by Plasmodium falciparum merozoites. Treatment of normal erythrocytes with trypsin and chymotrypsin also reduced invasion. Trypsinization of S-s- and En(a-) red cells, a process which removes the T1 peptide of glycophorins A and C, produced cells almost refractory to invasion. The human K562 erythroleukaemia cell line, which also expresses glycophorin A, was not invaded and possible explanations for this result are discussed. It is suggested that determinants carried on the red cell sialoglycoproteins (glycophorins A, B and C), in particular the T1 peptide of glycophorins A and C, play an essential role in attachment and invasion by P. falciparum merozoites. The oligosaccharide components found on this peptide may play a role in the initial binding between red cell and merozoites.
缺乏血型糖蛋白A(En(a-)细胞)和血型糖蛋白B(S-s-U-和S-s-U+细胞)的人类红细胞在体外对恶性疟原虫裂殖子的入侵表现出显著抗性。用胰蛋白酶和糜蛋白酶处理正常红细胞也会降低入侵率。对S-s-和En(a-)红细胞进行胰蛋白酶处理,该过程会去除血型糖蛋白A和C的T1肽,产生的细胞几乎对入侵具有抗性。同样表达血型糖蛋白A的人类K562红白血病细胞系未被入侵,并对该结果的可能解释进行了讨论。有人提出,红细胞唾液糖蛋白(血型糖蛋白A、B和C)上携带的决定簇,特别是血型糖蛋白A和C的T1肽,在恶性疟原虫裂殖子的附着和入侵中起重要作用。该肽上发现的寡糖成分可能在红细胞与裂殖子之间的初始结合中起作用。