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The role of JAM‐A and PECAM‐1 in modulating leukocyte infiltration in inflamed and ischemic tissues
Author(s) -
Nourshargh Sussan,
Krombach Fritz,
Dejana Elisabetta
Publication year - 2006
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.1105645
Subject(s) - biology , microbiology and biotechnology , infiltration (hvac) , endothelium , leukocyte trafficking , inflammation , cell adhesion molecule , in vivo , immunology , chemokine , genetics , physics , thermodynamics
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.