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Related Experiment Videos

DNAM-1 and PVR regulate monocyte migration through endothelial junctions.

Nicolas Reymond1, Anne-Marie Imbert, Elisabeth Devilard

  • 1Institut National de la Santé et de la Recherche Médicale UMR599, Institut de Cancérologie de Marseille, IFR 137, 27 Bd. Lei-Roure, 13009 Marseille, France.

The Journal of Experimental Medicine
|May 12, 2004
PubMed
Summary

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DNAX accessory molecule 1 (DNAM-1) binding to poliovirus receptor (PVR) on endothelial cells regulates monocyte extravasation. This interaction is crucial for monocytes migrating through blood vessel walls during inflammation.

Area of Science:

  • Immunology
  • Cell Biology
  • Vascular Biology

Background:

  • DNAX accessory molecule 1 (DNAM-1; CD226) is a key molecule in T and NK cell cytotoxicity.
  • DNAM-1 ligands, poliovirus receptor (PVR; CD155) and Nectin-2 (CD112), mediate cellular interactions.
  • Understanding DNAM-1's role in leukocyte trafficking is crucial for inflammatory and immune responses.

Purpose of the Study:

  • To investigate the expression of DNAM-1 ligands on endothelial cells.
  • To determine the role of the DNAM-1-PVR interaction in monocyte transendothelial migration.
  • To elucidate the mechanism of monocyte extravasation at endothelial junctions.

Main Methods:

  • Detection of PVR and Nectin-2 expression on primary vascular endothelial cells.
  • Binding assays using soluble DNAM-1-Fc and blocking antibodies (anti-PVR, anti-Nectin-2).

Related Experiment Videos

  • In vitro assays assessing monocyte transmigration through endothelial monolayers with antibody treatments.

    • Main Results:

    • PVR and Nectin-2 are expressed at cell junctions on vascular endothelial cells.
    • PVR is identified as the primary DNAM-1 ligand on endothelial cells, confirmed by antibody blocking studies.
    • DNAM-1-PVR interaction significantly inhibits monocyte transmigration, with monocytes arresting at endothelial junctions.

    Conclusions:

    • DNAM-1 regulates monocyte extravasation (diapedesis) through its interaction with PVR.
    • PVR expression at endothelial junctions is critical for this DNAM-1-mediated process.
    • This finding highlights a novel mechanism in leukocyte trafficking relevant to inflammatory diseases.