Published online before print July 20, 2006
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,
,¶,1
* Cardiovascular Medicine Unit, National Heart and Lung Institute, Imperial College London, London, United Kingdom;
Institute for Surgical Research, University of Munich, Munich, Germany;
FIRC Institute of Molecular Oncology, Milan Italy;
Department of Biomolecular and Biotechnological Sciences, School of Sciences, University of Milan, Milan, Italy; and
¶ Mario Negri Institute of Pharmacological Research, Milan, Italy
1 Correspondence: IFOM, FIRC Institute of Molecular Oncology, Via Adamello 16, Milan 20139, Italy. E-mail: elisabetta.dejana{at}ifom-ieo-campus.it
ABSTRACT
Innate and adaptive immunological responses are accompanied by leukocyte adhesion to the blood-vessel wall and their subsequent infiltration into the underlying tissues. In the majority of the cases, leukocytes cross the endothelium by squeezing through the border of apposed endothelial cells, a process that is known as diapedesis. Many data suggest that proteins at endothelial junctions establish homophilic interactions with identical proteins, which are present on leukocytes. These interactions might then direct the passage of leukocytes through the endothelial border. In this review, we focus on two endothelial junctional proteins [junctional adhesion molecule-A (JAM-A) and PECAM], which play an important role in leukocyte diapedesis. In vivo data with blocking antibodies or inactivation of JAM-A and PECAM genes indicate that the role of these two proteins depends on the stimulus and the experimental model used.
Key Words: inflammation • ischemia • endothelium
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