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Open access, freely available online Synopses of Research Articles Targeting of Endothelial Activation in Cerebral Malaria DOI: 10.1371/journal.pmed.0020315 Malaria is one of the most serious of all tropical parasitic diseases: a severe and life-threatening form of which in humans is cerebral malaria, a complication that can occur in malaria caused by Plasmodium falciparum.This grave complication involves malarial infection of the red blood cells that accumulate within the very small capillaries that ?ow through the tissues of the brain. Even when treated, cerebral malaria has a fatality rate of 15% or more. cell activation, adhesiveness for malarial parasites, and vesiculation. Using an in vitro model of cerebral malaria based on human,brain-derived endothelial cells (HBEC-5i),they found that LMP-420 potently reduced endothelial activation,endothelial adhesiveness for P.falciparum–parasitized red blood cells, and endothelial MP release,three major features of cerebral malaria. The results provide evidence for a dual inhibitory effect of LMP-420 on both TNF and LT in an in vitro model of cerebral malaria pathogenesis, when added either before or simultaneously with both cytokines, they said. LMP-420 also abolished the cytoadherence of ICAM-1-speci?c P. falciparum–parasitized red blood cells on these endothelial cells. Identical but weaker effects were observed when LMP-420 was added with LT. LMP-420 also caused a dramatic reduction of HBEC-5i vesiculation Numerous studies have pointed to a key role of tumor necrosis factor (TNF) and related proteins in the DOI: 10.1371/journal.pmed.0020315.g001 Plasmodium-infected red blood cells bind to brain endothelial cells pathogenesis of cerebral malaria, and a clear relationship has been established between plasma concentrations of TNF and cerebral pathology. In experimental cerebral malaria,TNF-beta, now called lymphotoxinα (LT), has been shown to be a principal mediator of pathogenesis. LT and TNF belong to the same