Glycophorins and Red Cell Invasion by Plasmodium falciparum
Geoffrey Pasvol, Michele Jungery
Abstract
Geoffrey Pasvol, Michele Jungery
Abstract
The major red cell sialoglycoproteins, the glycophorins, play a central role in the invasion of human red cells by Plasmodium falciparum. En(a-) cells deficient in glycophorin A (alpha) and S-s-U- cells deficient in glycophorin B (delta) are relatively resistant to invasion, while trypsin treatment of S-s-U- cells, which removes most of the remaining sialoglycoprotein, renders these cells almost totally resistant to invasion. Parasites inside these glycophorin-deficient cells develop normally. Invasion of erythroid precursors in vitro by merozoites of P. falciparum parallels the appearance of glycophorins on the surface of these nucleated cells, even though parasites fail to develop inside them. However, another type of cell from an erythroleukaemic line (K562) which expresses glycophorins on its surface is resistant to invasion. Furthermore, the observed increased invasion of young cells as opposed to an older cell population is not related quantitatively to the presence of glycophorins on the cell surface. Thus, although the role of glycophorins is both specific and important in the invasion of cells by P. falciparum, it is clearly only part of a complex process.
OpenAlex reports 33 citations for this work. Citation counts describe recorded attention and do not establish research quality.
A contribution statement is not available in the OpenAlex record.
Method details are not available in the OpenAlex metadata.
Findings are not separately available in the OpenAlex metadata.
Limitations are not available in the OpenAlex metadata.
Application details are not available in the OpenAlex metadata.
The major red cell sialoglycoproteins, the glycophorins, play a central role in the invasion of human red cells by Plasmodium falciparum. En(a-) cells deficient in glycophorin A (alpha) and S-s-U- cells deficient in glycophorin B (delta) are relatively resistant to invasion, while trypsin treatment of S-s-U- cells, which removes most of the remaining sialoglycoprotein, renders these cells almost totally resistant to invasion. Parasites inside these glycophorin-deficient cells develop normally. Invasion of erythroid precursors in vitro by merozoites of P. falciparum parallels the appearance of glycophorins on the surface of these nucleated cells, even though parasites fail to develop inside them. However, another type of cell from an erythroleukaemic line (K562) which expresses glycophorins on its surface is resistant to invasion. Furthermore, the observed increased invasion of young cells as opposed to an older cell population is not related quantitatively to the presence of glycophorins on the cell surface. Thus, although the role of glycophorins is both specific and important in the invasion of cells by P. falciparum, it is clearly only part of a complex process.
Key concepts: Glycophorin, Plasmodium falciparum, Biology, Parasite hosting, Immunology, Malaria, Computer science, Antigen