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Related Experiment Videos

Identification and characterisation of human Junctional Adhesion Molecule (JAM).

L A Williams1, I Martin-Padura, E Dejana

  • 1Cell Adhesion Laboratory, Institute of Molecular Medicine, University of Oxford, John Radcliffe Hospital, UK.

Molecular Immunology
|March 4, 2000
PubMed
Summary

Researchers identified a human Junctional Adhesion Molecule (JAM) involved in immune cell migration. This molecule is expressed on various circulating immune cells, suggesting a role in controlling leukocyte diapedesis and endothelial interactions.

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Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • Immune cell migration across intercellular junctions is crucial for immune responses.
  • Disruption of junctional structures during immune cell passage is of significant interest.
  • Understanding molecules at cell-cell contacts may reveal mechanisms controlling leukocyte diapedesis.

Purpose of the Study:

  • To describe the human orthologue to Junctional Adhesion Molecule (JAM).
  • To investigate the expression pattern of human JAM.
  • To explore the potential role of human JAM in leukocyte-endothelial interactions.

Main Methods:

  • Identification and characterization of the human JAM protein.
  • Analysis of JAM structure and sequence conservation with murine JAM.

Related Experiment Videos

  • Assessment of JAM expression on circulating immune cells.

    • Main Results:

    • The human JAM protein shares conserved structure and sequence with its murine counterpart.
    • Human JAM is constitutively expressed on circulating neutrophils, monocytes, platelets, and lymphocyte subsets.
    • This broad expression pattern is comparable to CD31, another intercellular junction molecule.

    Conclusions:

    • Human JAM is a novel immunoglobulin superfamily member expressed at intercellular junctions.
    • Its broad expression on circulating immune cells suggests a significant role in leukocyte diapedesis.
    • Human JAM may contribute to the complex regulation of leukocyte-endothelial interactions.