The role of JAM-A and PECAM-1 in modulating leukocyte infiltration in inflamed and ischemic tissues.
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.
Nourshargh
Sussan
S
National Heart and Lung Institute, Imperial College London, UK.
Krombach
Fritz
F
Dejana
Elisabetta
E
D000818:Animals; D015815:Cell Adhesion Molecules / Q000235:genetics / Q000276:immunology*; D006801:Humans; D007136:Immunoglobulins / Q000235:genetics / Q000276:immunology*; D007249:Inflammation / Q000276:immunology*; D007511:Ischemia / Q000276:immunology*; D007962:Leukocytes / Q000276:immunology*; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000235:genetics / Q000276:immunology*; D011956:Receptors, Cell Surface / Q000235:genetics / Q000276:immunology*
D015815:Cell Adhesion Molecules; C407243:F11R protein, human; C498686:F11r protein, mouse; D007136:Immunoglobulins; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D011956:Receptors, Cell Surface