ICAM-1 can play a major role in mediating P. falciparum adhesion to endothelium under flow.

We have investigated the importance of adhesion molecule co-operation in mediating Plasmodium falciparum adhesion to endothelial cells under flow conditions. Using three laboratory parasite lines and a patient isolate which differ in their ICAM-1 and CD36-binding avidity, we found that blockade of ICAM-1 and CD36 separately reduced IRBC adhesion by up to 95 and 50%, respectively. These results confirm previous data showing that ICAM-1 and CD36 synergize to mediate adhesion, but differ in demonstrating that without ICAM-1, binding under flow conditions is severely impaired. Thus, in this system, ICAM-1 is critical for P. falciparum adhesion to activated endothelium and once bound, synergy with CD36 mediates the majority (> or =98%) of adhesion.