VE-cadherin and PECAM-1 enhance ALL migration across brain microvascular endothelial cell monolayers

摘要

ObjectiveInfiltration of the central nervous system (CNS) by leukemia is a problematic disease manifestation of acute lymphoblastic leukemia (ALL). The mechanisms by which leukocytes interact with brain-derived microvasculature endothelial cells (HBMEnd) and enter the CNS are largely derived from models of inflammation. However, our data indicate that ALL cells do not elicit an inflammatory phenotype by HBMEnd. Our current investigation focuses on the contribution of the unique co-expression of VE-cadherin and PECAM-1 by ALL in mediating leukemic cell interactions with HBMEnd as an in vitro model of the blood-brain-barrier.