Killing of the malarial parasite Plasmodium yoelii in vitro by cells of myeloid origin.
Cytotoxic effects of mouse cells on Plasmodium yoelii were sought directly by incubating parasitized red cells with cells of various kinds for 16 h and then determining the percentage parasite survival in vivo, in terms of infectivity for the mouse. Cell populations rich in lymphocytes, e.g. lymph node and spleen, were less active than peritoneal cells and blood. Parasite killing by peritoneal cells was associated with macrophages: treatment with anti-macrophage serum (AMS) or depletion by adherence or centrifugation on Ficoll decreased activity. Polymorphonuclear leucocytes (PMN) in induced exudates may have contributed to killing, although not as actively cell for cell, and an effect of eosinophils in worm-induced exudates was not excluded. White blood cells were most active of all and fractionation on Ficoll confirmed that lymphocytes were relatively ineffective. The effector cell was phagocytic but it was insensitive to AMS. Tests on populations wih high or low proportions of PMN showed that parasite killing was independent of PMN number. It is concluded that the effector cell belongs to the monocyte-macrophage series and has acquired the ability to kill the parasite before becoming fully differentiated into a macrophage.
D000818:Animals; D001202:Ascitic Fluid / Q000166:cytology; D001854:Bone Marrow Cells; D003602:Cytotoxicity, Immunologic; D004804:Eosinophils / Q000276:immunology; D007106:Immune Sera / Q000494:pharmacology; D008214:Lymphocytes / Q000276:immunology; D008264:Macrophages / Q000276:immunology*; D051379:Mice; D009000:Monocytes / Q000276:immunology*; D009504:Neutrophils / Q000276:immunology; D010587:Phagocytosis; D010961:Plasmodium / Q000276:immunology*; D014357:Trypsin / Q000494:pharmacology
D007106:Immune Sera; D014357:Trypsin