A radical interpretation of immunity to malaria parasites.
Asexual forms of malaria parasites in erythrocytes are sensitive to oxidant stress. Immunity to these parasites is thymus-dependent and may be mediated by the blinding of effector cells (macrophages or natural killer cells) to the surface of parasitised cells, with concomitant production of the superoxide anion (O2-). This can lead to degeneration of parasites in erythrocytes. Antibodies can facilitate the binding of effector cells to parasitised erythrocytes, reinforcing the effects of cell-mediated immunity. Plasmodium falciparum is more sensitive to oxidant stress in human erythrocytes with abnormal haemoglobins and glucose-6-phosphate-dehydrogenase deficiency than in normal erythrocytes. Thus cell-mediated immune responses, by producing oxidant stress, could act synergistically with these inherited traits to increase the chances of survival of children during the dangerous years of first exposure to malaria.
D000917:Antibody Formation; D002648:Child; D004912:Erythrocytes / Q000378:metabolism* / Q000469:parasitology; D006801:Humans; D007111:Immunity, Cellular; D007694:Killer Cells, Natural / Q000276:immunology; D008264:Macrophages / Q000276:immunology; D008288:Malaria / Q000097:blood / Q000276:immunology*; D008954:Models, Biological; D010084:Oxidation-Reduction; D010961:Plasmodium / Q000378:metabolism; D013481:Superoxides / Q000378:metabolism
D013481:Superoxides