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Real-time Imaging of Endothelial Cell-cell Junctions During Neutrophil Transmigration Under Physiological Flow
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Molecular mechanisms that control leukocyte extravasation through endothelial cell contacts

D Vestweber1

  • 1Max Planck Institute of Molecular Biomedicine, Röntgenstr. 20, 48149 Münster, Germany. vestweb@mpi-muenster.mpg.de

Ernst Schering Foundation Symposium Proceedings
|May 31, 2008
PubMed

Leukocyte extravasation and entry into tissue forms the basis for inflammatory reactions and lymphocyte surveillance. After docking at the blood vessel wall at sites of exit leukocytes migrate through the endothelial cell layer and the underlying basement membrane, a process described as diapedesis. In recent years, several endothelial membrane proteins that which participate in this process have been identified. This review focuses on three membrane proteins located at endothelial cell contacts that are involved in the regulation of leukocyte diapedesis. The endothelial cell selective adhesion molecule (ESAM) at endothelial tight junctions and the vascular endothelial receptor-type protein tyrosine phosphatase (VE-PTP), a protein associating with VE-cadherin, both seem to control the integrity of endothelial cell contacts during diapedesis. CD99 and the distantly related CD99L2 are leukocyte membrane proteins that do not belong to any known protein family. They are expressed at endothelial cell contacts and participate in the migration of leukocytes through endothelium and basement membrane.

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