The Role of JAM-A and PECAM-1 in Modulating Leukocyte Infiltration in Inflamed and Ischemic Tissues

J Leukoc Biol. 2006 Oct;80(4):714-8. doi: 10.1189/jlb.1105645. Epub 2006 Jul 20.

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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Cell Adhesion Molecules / genetics
  • Cell Adhesion Molecules / immunology*
  • Humans
  • Immunoglobulins / genetics
  • Immunoglobulins / immunology*
  • Inflammation / immunology*
  • Ischemia / immunology*
  • Leukocytes / immunology*
  • Platelet Endothelial Cell Adhesion Molecule-1 / genetics
  • Platelet Endothelial Cell Adhesion Molecule-1 / immunology*
  • Receptors, Cell Surface / genetics
  • Receptors, Cell Surface / immunology*

Substances

  • Cell Adhesion Molecules
  • F11R protein, human
  • F11r protein, mouse
  • Immunoglobulins
  • Platelet Endothelial Cell Adhesion Molecule-1
  • Receptors, Cell Surface