Red blood cells are protected from attack by natural killer cells
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Peer-reviewed studies indicate that normal, uninfected red blood cells remain intact and are protected from destruction by natural killer cells, with specific membrane proteins contributing to this resistance.
Glycophorin A is a protein with an abundant glycosylation (60% carbohydrate by weight), and studies have suggested that resistance of target cells to natural killing may be correlated with the level of glycophorin A expression. To assess the role of glycophorin A and of its carbohydrates in sensitivity to lysis by natural killer (NK) cells, the glycoprotein was inserted into the membrane of K562 target cells using electropulsation. Peripheral blood lymphocytes were used as effector cells. When glycophorin A was inserted into the membrane, the level of resistance to NK cell attack increased with the number of glycophorin A molecules electroinserted. The resistance to lysis was not due to a defect in target cell-effector cell binding. Electroassociation of glycophorin A did not cause a decrease in the expression of either “positive signals” for NK cells (such as CD71, CD15, and CD32 antigens) or cellular adhesion molecules (CD18, CD29, CD54, and CD58). Furthermore, electroinsertion of glycophorin A did not trigger any “negative signals,” such as class I HLA antigen expression. Finally, it was shown that the sialic acid and O-linked oligosaccharides of glycophorin A did not play any role in its effect against NK cells. Conversely, the unique N-linked oligosaccharide was shown to be essential for resistance to occur.
antibodies bind to infected cells flagging them for destruction by cells of the immune system. Immune cells called natural killer cells can eliminate viruses or cancer cells this way, but it was not clear if they could also eliminate malaria parasite-infected red blood cells.
Now, Arora et al. show that natural killer cells can selectively destroy malaria-infected red blood cells flagged with antibodies from people who live in areas where malaria is common. In laboratory experiments, natural killer cells from US volunteers, who were never exposed to malaria, did not kill normal or malaria-infected red blood cells. Adding antibodies collected from malaria-resistant volunteers from Africa allowed these natural killer cells from unexposed people to selectively seek out and destroy malaria-infected cells and leave uninfected red blood cells intact.
Arora et al. also found that the antibodies from the malaria-resistant volunteers bound to parasite proteins on the surface of infected blood cells. The experiments suggest that vaccines designed to stimulate the production of antibodies to malaria proteins that are displayed on infected red blood cells, could destroy the parasite in infected people and help prevent disease and save lives. Introduction
Plasmodium falciparum (P. falciparum.) , the causative agent of malaria, expresses proteins that are displayed at the surface of infected red blood cells (RBCs). Some of these proteins promote sequestration of P.f.- infected RBCs (iRBCs) through adhesion to vascular endothelial cells ( Miller et al., 2002 ). Humans living in malaria-endemic areas generate, over years of repeated infections, antibodies (Abs) to P.f . proteins that contribute to the gradual protection from malaria symptoms ( Boyle et al., 2015 ; Bull and Marsh, 2002 ; Cohen et al., 1961 ; Mayor et al., 2015 ; Tran et al., 2013 ). One of the main objectives in malaria research is to define the mechanisms by which naturally acquired Abs provide protection ( Cohen e
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