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Related Experiment Videos

Junctional adhesion molecule-2 (JAM-2) promotes lymphocyte transendothelial migration.

Caroline A Johnson-Léger1, Michel Aurrand-Lions, Nicola Beltraminelli

  • 1Department of Pathology, University Medical Centre, 1, Rue Michel-Servet, Geneva, Switzerland. caroline.johnson-leger@medecine.unige.ch

Blood
|September 20, 2002
PubMed
Summary

Junctional adhesion molecule-2 (JAM-2) facilitates lymphocyte movement across blood vessel walls. Blocking JAM-2 inhibits leukocyte migration, revealing its crucial role in immune cell trafficking.

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Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • Lymphocyte extravasation, the process of immune cells moving into tissues, is critical for immune responses but not fully understood.
  • High endothelial venules (HEVs) are specialized blood vessels facilitating lymphocyte entry into lymphoid organs.
  • Junctional adhesion molecule-2 (JAM-2) was recently identified and initially observed on mouse HEVs.

Purpose of the Study:

  • To investigate the role of JAM-2 in lymphocyte extravasation.
  • To determine if JAM-2 mediates leukocyte transmigration across endothelial cells.
  • To identify and characterize the human homologue of JAM-2 and its function in leukocyte trafficking.

Main Methods:

  • Antibody staining of mouse lymph nodes and Peyer patches to detect JAM-2.

Related Experiment Videos

  • In vitro migration assays using mouse lymphocytes and JAM-2 transfected endothelioma cells.
  • Cloning of human JAM-2.
  • Transmigration assays using human peripheral blood leukocytes and human umbilical vein endothelial cells (HUVECs).
  • Immunofluorescence staining for JAM-2 on human tonsil HEVs and leukocytes.

    • Main Results:

    • Antibodies to mouse JAM-2 stained HEVs in lymphoid tissues.
    • Mouse lymphocytes showed increased migration across JAM-2 expressing endothelioma cells.
    • Human JAM-2 was cloned and characterized.
    • Anti-JAM-2 antibodies and soluble JAM-2 blocked human leukocyte transmigration across HUVECs.
    • JAM-2 was detected on human tonsil HEVs and a subset of human leukocytes.

    Conclusions:

    • JAM-2 promotes lymphocyte migration across endothelial barriers.
    • JAM-2 is expressed on HEVs in both mice and humans, suggesting conserved function.
    • JAM-2 plays a significant role in regulating leukocyte transendothelial migration in humans.
    • JAM-2 represents a potential therapeutic target for modulating immune cell trafficking.