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Central to the pathologic progression of human cerebral malaria (CM) is sequestration of Plasmodium falciparum-infected red blood cells (Pf-IRBCs) to the blood-brain barrier (BBB) endothelium. The molecular interactions between Pf-IRBCs and the BBB endothelium and their implications for barrier function are unclear.

Plasmodium falciparum–Infected Erythrocytes Decrease the Integrity of Human Blood‐Brain Barrier Endothelial Cell Monolayers