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Correspondence: Marilyn Telen, MD, Duke Univ. Med. Ctr., Division of Hematology, Box 2615, Durham, NC 27710–0001; phone (919) 684–5378; fax (919) 681–7688; telen002{at}mc.duke.edu
Abstract
A number of lines of evidence now support the hypothesis that vaso-occlusion and several of the sequelae of sickle cell disease (SCD) arise, at least in part, from adhesive interactions of sickle red blood cells, leukocytes, and the endothelium. Both experimental and genetic evidence provide support for the importance of these interactions. It is likely that future therapies for SCD might target one or more of these interactions.
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