Blockade of Adhesion of Sickle Cells to Endothelium by Monoclonal Antibodies

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Abstract
Red cells that contain sickle hemoglobin tend to acquire an abnormal, sickled shape when their mutant hemoglobin polymerizes as a result of low oxygen tension. In the classic view of sickle cell disease pathophysiology, it is this deoxygenation-induced sickling of red cells that plugs blood vessels, precipitating a vaso-occlusive event, which is most commonly manifested clinically as an acute painful episode. This simple concept belies the complexity of vaso-occlusion in sickle cell disease, as shown by research over the past two decades, which has added to our understanding of the problem. It is now recognized that additional factors probably contribute . . .