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Updated: Jan 29, 2026

In Vitro Stimulation and Visualization of Extracellular Trap Release in Differentiated Human Monocyte-derived Macrophages
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Ionizing Radiation Induces Extracellular Trap Release from Macrophages.

Yongchan Lee1, Monowar Aziz1,2, Ping Wang1,2

  • 1Center for Immunology and Inflammation, The Feinstein Institutes for Medical Research, 350 Community Dr., Manhasset, NY 11030, USA.

International Journal of Molecular Sciences
|January 28, 2026
PubMed
Summary

Ionizing radiation exposure triggers macrophages to release extracellular traps (METs) through pyroptosis, a cell death process. Targeting these radiation-induced METs may offer new strategies to reduce tissue injury.

Keywords:
Gasdermin DMETsPAD2PAD4extracellular trapsmacrophageradiation

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Area of Science:

  • Immunology
  • Cell Biology
  • Radiation Biology

Background:

  • Macrophages are crucial innate immune cells for pathogen defense.
  • Ionizing radiation can disrupt macrophage functions and worsen tissue damage.
  • Macrophage Extracellular Traps (METs) are released upon stimulation and play a role in immune responses.

Purpose of the Study:

  • To investigate if ionizing radiation exposure induces macrophages to release extracellular traps.
  • To elucidate the mechanisms underlying radiation-induced MET formation.
  • To explore the potential of targeting METs for mitigating radiation-induced tissue injury.

Main Methods:

  • Collected peritoneal macrophages from C57BL/6 mice.
  • Exposed macrophages to 5 Gy ionizing radiation.
  • Assessed MET formation using immunofluorescence for citrullinated histone H3 and cell-free DNA measurements.
  • Analyzed cell death pathways, including pyroptosis mediated by Gasdermin D (GSDMD).
  • Investigated the role of peptidyl arginine deiminase (PAD) 2 and 4 in MET formation.

Main Results:

  • Ionizing radiation induced significant macrophage death via GSDMD-mediated pyroptosis.
  • Pyroptosis led to both suicidal and vital METosis.
  • Radiation exposure increased MET formation, evidenced by elevated citrullinated histone H3 and extracellular DNA.
  • PAD 2 and 4 were essential for radiation-induced MET generation.

Conclusions:

  • Ionizing radiation induces macrophage extracellular trap formation through GSDMD activation and pyroptosis.
  • PAD enzymes are critical for METosis following radiation exposure.
  • Targeting METs presents a potential therapeutic avenue for managing radiation-induced tissue damage.