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Updated: Aug 20, 2025

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

Published on: August 14, 2014

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Neutrophil breaching of the blood vessel pericyte layer during diapedesis requires mast cell-derived IL-17A

Régis Joulia1,2, Idaira María Guerrero-Fonseca1,3, Tamara Girbl1,4

  • 1William Harvey Research Institute, Faculty of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London, EC1M 6BQ, UK.

Nature Communications
|November 17, 2022
PubMed

Insights

Perivascular mast cells (MCs) guide neutrophils to exit blood vessels by releasing IL-17A, a crucial step in inflammation. This MC-IL-17A-pericyte pathway impacts neutrophil diapedesis in inflammatory diseases.

Area of Science:

  • Immunology
  • Cell Biology
  • Vascular Biology

Background:

  • Neutrophil diapedesis is critical for immune responses to infection and injury.
  • Leukocyte interactions with the blood vessel wall govern neutrophil extravasation.
  • The sub-endothelial migration of neutrophils remains incompletely understood.

Purpose of the Study:

  • To investigate the role of perivascular mast cells (MCs) in neutrophil behavior within the sub-endothelial space.
  • To elucidate the molecular mechanisms regulating neutrophil migration towards blood vessel walls.
  • To identify novel pathways modulating neutrophil diapedesis.

Main Methods:

  • Confocal intravital microscopy to visualize neutrophil motility in vivo.
  • Utilizing MC-deficient models and pharmacological/genetic blockade of IL-17A.
  • Assessing the expression of effector molecules ICAM-1 and CXCL1 in pericytes.

Main Results:

  • Perivascular MCs direct neutrophil migration towards themselves in the sub-endothelial space.
  • MC deficiency or IL-17A blockade impairs neutrophil sub-endothelial migration and extravasation.
  • Mast cells are a significant source of IL-17A, which acts on pericytes to enhance ICAM-1 and CXCL1.

Conclusions:

  • A novel MC-IL-17A-pericyte axis regulates the final steps of neutrophil diapedesis.
  • This pathway is crucial for neutrophil extravasation at sites of inflammation.
  • Targeting this axis may offer therapeutic strategies for inflammatory disorders.

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