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Preparation of Myeloid Derived Suppressor Cells MDSC from Naive and Pancreatic Tumor-bearing Mice using Flow Cytometry and Automated Magnetic Activated Cell Sorting AutoMACS
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TMPRSS11D/ALR-mediated ER stress regulates the function of myeloid-derived suppressor cells in the cervical cancer

Sifang Feng1, Juan Zhao2, Ting Yang2

  • 1Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061, China.

International Immunopharmacology
|September 4, 2023
PubMed

Insights

Transmembrane serine protease 11D (TMPRSS11D) promotes cervical cancer immune evasion by enhancing myeloid-derived suppressor cell (MDSC) immunosuppression. Silencing TMPRSS11D reduces tumor growth and MDSC accumulation, offering a potential therapeutic target.

Area of Science:

  • Immunology
  • Oncology
  • Molecular Biology

Background:

  • Myeloid-derived suppressor cells (MDSCs) are key players in tumor immune evasion, particularly in cervical cancer.
  • The role of Transmembrane serine protease 11D (TMPRSS11D) in cervical cancer's immune escape remains largely unknown.
  • Understanding TMPRSS11D's mechanism in MDSC immunosuppression is crucial for developing novel cancer therapies.

Purpose of the Study:

  • To investigate the regulatory mechanism of TMPRSS11D on the immunosuppressive function of MDSCs in cervical cancer.
  • To determine if TMPRSS11D influences MDSC-mediated T cell inhibition.
  • To explore TMPRSS11D's impact on cervical cancer progression in vivo.

Main Methods:

  • Comparative analysis of MDSC markers and TMPRSS11D expression in cervical cancer patients versus benign tumor patients.
  • In vitro co-culture assays of T cells and MDSCs with TMPRSS11D knockdown.
  • Assessment of reactive oxygen species (ROS) production, T cell proliferation, and IFN-γ levels.
  • In vivo mouse xenograft models to evaluate TMPRSS11D's effect on tumor growth and MDSC infiltration.

Main Results:

  • Malignant cervical cancer patients exhibited higher PMN-MDSC proportions, immunosuppressive factors, and TMPRSS11D mRNA levels.
  • TMPRSS11D knockdown in MDSCs reduced ROS production and hindered their immunosuppressive capacity on T cells.
  • TMPRSS11D negatively regulated ALR expression, induced ER stress in MDSCs, and promoted cervical cancer growth in vivo.

Conclusions:

  • TMPRSS11D enhances MDSC-mediated immunosuppression in cervical cancer by inducing ER stress via ALR downregulation.
  • Targeting TMPRSS11D may represent a promising strategy to overcome immune evasion and inhibit cervical cancer progression.
  • Further research into TMPRSS11D's molecular pathways could reveal new therapeutic avenues for cervical cancer treatment.
Keywords:
ALRCervical cancerER stressMDSCsTMPRSS11D

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