Glycophorin as a possible receptor for Plasmodium falciparum.
Human red cells deficient in glycophorin B are partly resistant to invasion by Plasmodium falciparum and become completely resistant when glycophorin A is removed from their surface by trypsin treatment. Similar treatment of cells which have a hybrid glycophorin molecule renders them glycophorin-deficient and resistant to invasion. Tn and Wrb -ve cells with defined alterations in glycophorin A or B are also resistant to invasion. These findings suggest that both glycophorins A and B are involved in parasite invasion, indicate which parts of these molecules may be involved in this process, and provide the basis for a tentative model of parasite/red-cell interactions.
D001789:Blood Group Antigens / Q000187:drug effects; D004910:Erythrocyte Membrane / Q000378:metabolism / Q000469:parasitology*; D004912:Erythrocytes / Q000469:parasitology*; D006021:Glycophorins / Q000502:physiology*; D006801:Humans; D008954:Models, Biological; D010963:Plasmodium falciparum / Q000187:drug effects / Q000378:metabolism*; D011971:Receptors, Immunologic / Q000276:immunology*; D012795:Sialoglycoproteins / Q000502:physiology*; D014357:Trypsin / Q000494:pharmacology
D001789:Blood Group Antigens; D006021:Glycophorins; D011971:Receptors, Immunologic; D012795:Sialoglycoproteins; D014357:Trypsin