Putative pathophysiological interactions of cytokines and phagocytic cells in severe human falciparum malaria.
The severe disease and high mortality associated with Plasmodium falciparum infection have traditionally been attributed solely to parasitic virulence factors, but more recent evidence suggests that the host's immunologic response may also contribute to the pathophysiology of the disease in humans. This response would be expected to be proportionate--in intensity and nature--to the antigenic load created by the sequestration of parasites in the microvasculature and to be directed against the sites of maximal parasitization; thus the immunologic response could potentially contribute to the pathophysiology of both survival and fatal outcome in severe infection. Cytokines appear to play a pivotal role in the activation of the immune response in human falciparum malaria, and their levels correlate with disease severity. The putative mechanisms by which cytokines may mediate both beneficial and deleterious effects by activating phagocytic cells in severe falciparum malaria are discussed.
Urquhart
A D
AD
St. Peter's College, Oxford University Medical School, United Kingdom.
D016207:Cytokines / Q000276:immunology* / Q000378:metabolism; D006801:Humans; D007111:Immunity, Cellular; D008264:Macrophages / Q000276:immunology / Q000378:metabolism; D016778:Malaria, Falciparum / Q000276:immunology* / Q000503:physiopathology; D010587:Phagocytosis / Q000276:immunology*; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology / Q000378:metabolism
D016207:Cytokines; D014409:Tumor Necrosis Factor-alpha