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We have investigated the widely held view that malaria parasites induce pro-inflammatory cytokines primarily through an endotoxin-like stimulatory effect on macrophages. We report that the pattern of cytokine production by non-immune human peripheral blood mononuclear cells following stimulation by Plasmodium falciparum-infected erythrocytes (Pfe) in vitro differs considerably from that induced by bacterial endotoxin. The Pfe-induced TNF response at day 1 is associated with a much higher level of IFN-gamma production and a much lower level of IL-12 p40 and IL-10 expression than a comparable endotoxin-induced TNF response. Both CD3(+) and CD14(+) populations are required for this early TNF response to Pfe, whereas the endotoxin-induced response is unaffected by depletion of the CD3(+) population. Pfe fails to stimulate the monocyte-like cell line MonoMac6 to express pro-inflammatory cytokines. These findings suggest that the early inflammatory response to malaria is critically dependent on lymphocyte subpopulations that play a lesser role in the response to bacterial endotoxin.

Original publication




Journal article


European journal of immunology

Publication Date





2636 - 2644


Oxford University Department of Paediatrics, John Radcliffe Hospital, Oxford, GB.


Erythrocytes, Leukocytes, Mononuclear, Animals, Humans, Plasmodium falciparum, Lipopolysaccharides, Tumor Necrosis Factor-alpha, RNA, Messenger, DNA Primers, Cytokines, Gene Expression, Base Sequence, Kinetics, In Vitro Techniques, CD3 Complex, Lipopolysaccharide Receptors