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Junctional adhesion molecule-C regulates the early influx of leukocytes into tissues during inflammation

Michel Aurrand-Lions1, Chrystelle Lamagna, John P Dangerfield

  • 1Department of Pathology and Immunology, Medical University Center, Geneva, Switzerland. Michel.Aurrand-Lions@medecine.unige.ch

Journal of Immunology (Baltimore, Md. : 1950)
|May 10, 2005
PubMed

Insights

Junctional adhesion molecule (JAM)-C regulates leukocyte migration to inflammatory sites. Blocking JAM-C partially inhibited leukocyte accumulation, while overexpression increased it, highlighting its role in later adhesion steps.

Area of Science:

  • Immunology
  • Cell Biology
  • Inflammation Research

Background:

  • Leukocyte recruitment to inflammatory sites is a multistep process involving molecular interactions.
  • Junctional adhesion molecule (JAM)-C is expressed on endothelial cells and may regulate neutrophil migration via interaction with leukocyte integrin Mac-1.

Purpose of the Study:

  • To investigate the role of JAM-C in leukocyte recruitment during acute pulmonary inflammation.
  • To elucidate the specific mechanisms by which JAM-C influences leukocyte migration in vivo.

Main Methods:

  • Utilized neutralizing antibodies against JAM-C to block leukocyte accumulation in mouse lungs.
  • Generated transgenic mice overexpressing JAM-C under the Tie2 promoter for in vivo studies.
  • Employed intravital microscopy to observe leukocyte-endothelial interactions.

Main Results:

  • Neutralizing antibodies against JAM-C partially blocked leukocyte accumulation in alveoli during pulmonary inflammation.
  • Transgenic mice overexpressing JAM-C showed increased leukocyte accumulation at inflammatory sites.
  • Intravital microscopy revealed increased leukocyte adhesion and transmigration in transgenic mice, with no significant effect on rolling.

Conclusions:

  • JAM-C plays a significant role in regulating leukocyte recruitment to inflammatory sites.
  • JAM-C is involved in the later stages of the leukoendothelial adhesion cascade, specifically adhesion and transmigration.
  • Targeting JAM-C may offer therapeutic potential for inflammatory conditions.

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