Plasmodium falciparum is a global health problem because of the morbidity and mortality associated with infection. Much of this morbidity and mortality is believed to arise from the actions of a malaria toxin. The toxin initiates a systemic inflammatory cascade involving cytokine excess, which may result in disseminated intravascular coagulation, hepatic dysfunction, acute renal failure, multi-organ inflammation, hypoglycemia, lactic acidosis and death. The toxin may further contribute to organ-specific and cerebral disease syndromes by hyperactivation of the vascular endothelium. Clinical immunity to malaria is acquired considerably earlier than anti-parasite immunity, and it is possible that this is mediated by anti-toxin mechanisms.
| Hansen, Diana S; D'Ombrain, Marthe C; Schofield, Louis (2007) The role of leukocytes bearing Natural Killer Complex receptors and Killer Immunoglobulin-like Receptors in the immunology of malaria. Curr Opin Immunol 19:416-23 |
| D'Ombrain, Marthe C; Hansen, Diana S; Simpson, Ken M et al. (2007) gammadelta-T cells expressing NK receptors predominate over NK cells and conventional T cells in the innate IFN-gamma response to Plasmodium falciparum malaria. Eur J Immunol 37:1864-73 |
