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Simultaneous Study of the Recruitment of Monocyte Subpopulations Under Flow In Vitro
Published on: November 26, 2018
JAM-C regulates unidirectional monocyte transendothelial migration in inflammation
Paul F Bradfield1, Christoph Scheiermann, Sussan Nourshargh
1Department of Pathology and Immunology, University Medical Centre, Geneva, Switzerland.
Blood
|July 13, 2007
Summary
Blocking the interaction between Junctional Adhesion Molecule-B (JAM-B) and JAM-C reduces monocyte accumulation at inflammation sites. This occurs by promoting reverse transmigration, not by inhibiting initial transmigration.
Area of Science:
- Immunology
- Cell Biology
- Vascular Biology
Background:
- Monocyte recruitment is crucial for inflammatory responses.
- Junctional Adhesion Molecule-C (JAM-C) is implicated in monocyte transmigration across endothelial barriers.
- Understanding the regulation of monocyte extravasation is key to controlling inflammation.
Purpose of the Study:
- To investigate the role of JAM-B/-C interactions in monocyte recruitment.
- To explore the impact of blocking JAM-B/-C on monocyte transmigration and retention at inflammation sites.
Main Methods:
- Utilized blockade of JAM-B/-C interactions.
- Assessed monocyte transmigration and reverse transmigration.
- Employed in vivo models to confirm findings in an inflammatory context.
Main Results:
- Blockade of JAM-B/-C interaction increased reverse transmigration of monocytes.
- This blockade led to reduced monocyte numbers in the extravascular compartment.
- An anti-JAM-C antibody decreased monocytes in inflammatory tissue and increased those with a reverse-transmigratory phenotype in blood.
Conclusions:
- Disrupting JAM-C-mediated monocyte retention offers a novel strategy to reduce inflammatory cell accumulation.
- Targeting JAM-B/-C interactions can modulate monocyte trafficking during inflammation.
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