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Real-time Imaging of Endothelial Cell-cell Junctions During Neutrophil Transmigration Under Physiological Flow
11:26

Real-time Imaging of Endothelial Cell-cell Junctions During Neutrophil Transmigration Under Physiological Flow

Published on: August 14, 2014

CD99 and CD99L2 act at the same site as, but independently of, PECAM-1 during leukocyte diapedesis

M Gabriele Bixel1, Hang Li, Bjoern Petri

  • 1Max Planck Institute of Molecular Biomedicine, Roentgenstrasse 20, Münster, Germany.

Blood
|May 19, 2010
PubMed

Insights

Mouse CD99 and CD99L2 molecules cooperate independently of PECAM-1 to facilitate neutrophil extravasation. These adhesion molecules are crucial for neutrophils to cross the endothelial basement membrane during inflammation.

Area of Science:

  • Immunology
  • Cell Biology
  • Vascular Biology

Background:

  • Leukocyte extravasation is a critical process in inflammation, mediated by adhesion receptors on endothelial cells.
  • The roles of CD99, CD99L2, and PECAM-1 in leukocyte trafficking are complex and require further elucidation.

Purpose of the Study:

  • To investigate the cooperative functions of mouse CD99, CD99L2, and PECAM-1 in leukocyte extravasation.
  • To determine the independent or cooperative roles of these molecules in neutrophils transmigrating the endothelial barrier.

Main Methods:

  • In vitro transmigration assays using antibodies against CD99 and PECAM-1.
  • In vivo studies utilizing electron microscopy and 3D confocal fluorescence microscopy in inflamed cremaster tissue.
  • Gene disruption of PECAM-1 and blocking antibodies against CD99 and CD99L2 in various inflammatory models (IL-1β and TNF-α).

Main Results:

  • Antibodies against CD99 and PECAM-1 trapped neutrophils between endothelial cells in vitro, but no sequential function was observed.
  • In vivo, blocking CD99/CD99L2 or PECAM-1 gene disruption trapped neutrophils between endothelial cells and the basement membrane.
  • PECAM-1 disruption and CD99/CD99L2 blockade inhibited extravasation in IL-1β-inflamed tissues.
  • CD99 and CD99L2 were essential for extravasation in TNF-α-stimulated cremaster, independent of PECAM-1.

Conclusions:

  • CD99 and CD99L2 act independently of PECAM-1 during leukocyte extravasation.
  • CD99 and CD99L2 cooperate to facilitate neutrophil transmigration across the endothelial basement membrane.
  • These findings highlight distinct pathways involved in leukocyte trafficking during inflammation.

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