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Immune checkpoints in the tumor microenvironment.

Salman M Toor1, Varun Sasidharan Nair1, Julie Decock1

  • 1Cancer Research Center, Qatar Biomedical Research Institute (QBRI), Hamad Bin Khalifa University (HBKU), Qatar Foundation (QF), PO Box 34110, Doha, Qatar.

Seminars in Cancer Biology
|July 3, 2019
PubMed
Summary
This summary is machine-generated.

Immune checkpoints (ICs) and their ligands hinder anti-tumor immunity. Targeting these pathways with inhibitors shows promise, but tumors develop resistance, necessitating further research into overcoming these barriers.

Keywords:
Immune checkpoint inhibitorsImmune checkpointsTumor microenvironment

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Area of Science:

  • Immunology
  • Oncology
  • Cancer Research

Background:

  • Immune checkpoints (ICs) and ligands negatively regulate T cell activation.
  • These pathways are upregulated in the tumor microenvironment (TME), impeding anti-tumor immune responses.
  • While immune checkpoint inhibitors (ICIs) are approved for cancer treatment, tumors can develop resistance.

Purpose of the Study:

  • To review the expression and impact of ICs/ligands in the TME on tumor immune evasion.
  • To discuss regulatory mechanisms (genetic, epigenetic, hypoxia, immunosuppressive cells) causing IC upregulation.
  • To explore the prognostic significance of ICs/ligands and strategies to enhance ICI treatment responses.

Main Methods:

  • Literature review of immune checkpoints, ligands, and their role in the tumor microenvironment.
  • Analysis of regulatory mechanisms contributing to immune checkpoint upregulation in various cancers.
  • Examination of prognostic significance and therapeutic strategies for immune checkpoint inhibition.

Main Results:

  • ICs and ligands are frequently upregulated in the TME, acting as barriers to effective anti-tumor immunity.
  • Tumor cells employ various strategies, including expression of additional ICs/ligands, to counteract ICI therapy.
  • Genetic, epigenetic factors, hypoxia, and immunosuppressive cells contribute to IC upregulation in cancers.

Conclusions:

  • Understanding ICs/ligands in the TME is crucial for advancing cancer immunotherapy.
  • Targeting ICs offers clinical benefits, but resistance mechanisms require further investigation.
  • Developing strategies to overcome tumor-induced resistance to ICIs is essential for improving patient outcomes.