Killing of Plasmodium falciparum by cytokine activated effector cells (neutrophils and macrophages).

Macrophages display natural antibody independent killing of asexual blood stages of Plasmodium falciparum in vitro. In contrast, the neutrophil killing of P. falciparum requires the presence of antibodies. Cytokines such as TNF alpha have very little effect on the macrophage-induced antiplasmodial activity, but significantly increase the damage of parasites by neutrophils. Cytokines, TNF alpha, IFN-gamma and TNF beta at very high concentrations were not toxic to P. falciparum in culture. It is postulated that the basis for cytokine modulated antiplasmodial activity of leukocytes is increased expression of Fc and complement receptors, which leads to a more efficient interaction between the parasite and neutrophils. It is also postulated that the parasite evades natural macrophage killing mechanisms by inducing factors which suppress this macrophage activity. Cytokine inhibitors may be induced during the course of a malarial infection. These could be involved in attempts to attain a balance between the host and the parasite, by protecting the parasite from the damaging effect of the immune system and protecting the host from the deleterious effects of cytokines.