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Updated: Jun 9, 2025

Screening Bioactive Nanoparticles in Phagocytic Immune Cells for Inhibitors of Toll-like Receptor Signaling
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CMTM3 regulates neutrophil activation and aggravates sepsis through TLR4 signaling

Haiyan Xue1,2,3, Ziyan Xiao1, Xiujuan Zhao1

  • 1Department of Critical Care Medicine, Peking University People's Hospital, Beijing, China.

EMBO Reports
|October 25, 2024
PubMed

Insights

Targeting CMTM3 protein in sepsis shows promise. Reducing CMTM3 improves survival rates and reduces organ damage by regulating neutrophil migration, offering a potential new therapy for sepsis management.

Area of Science:

  • Immunology
  • Molecular Biology
  • Pathophysiology

Background:

  • Neutrophil activation is critical in sepsis management.
  • CMTM3 (CKLF-like MARVEL transmembrane domain containing 3) is a membrane protein involved in immune responses.
  • Elevated CMTM3 expression is observed in sepsis.

Purpose of the Study:

  • To investigate the role of CMTM3 in sepsis-induced neutrophil migration.
  • To explore CMTM3 as a potential therapeutic target for sepsis.

Main Methods:

  • Utilized Cmtm3 knockout mouse models.
  • Analyzed neutrophil migration patterns.
  • Assessed inflammatory responses and organ damage markers.
  • Investigated the molecular mechanisms involving TLR4 and CXCR2.

Main Results:

  • Cmtm3 knockout significantly improved survival rates in septic mice.
  • Deletion of Cmtm3 mitigated inflammatory responses and ameliorated organ damage.
  • CMTM3 deficiency reduced Toll-like receptor 4 (TLR4) and C-X-C motif chemokine receptor 2 (CXCR2) expression on neutrophils, decreasing their migration.

Conclusions:

  • CMTM3 plays a key role in sepsis-associated neutrophil migration imbalance.
  • Targeting CMTM3 offers a potential therapeutic strategy to manage neutrophil dysregulation and multi-organ damage in sepsis.
Keywords:
CMTM3InflammationNeutrophilSepsis

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