PD-1 and its ligands are important immune checkpoints in cancer

Yinan Dong1, Qian Sun1, Xinwei Zhang1

  • 1Cell Immunology Laboratory, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin Key Laboratory of "Cancer Prevention and Therapy", Key Laboratory of Immunology and Cancer Biotherapy, Tianjin, China.

Oncotarget
|December 16, 2016
PubMed

Insights

The programmed death-1 (PD-1) and programmed cell death ligands (PD-Ls) pathway helps tumors evade immune attack. Blocking this pathway enhances anti-tumor immunity by restoring T-cell activity.

Area of Science:

  • Immunology
  • Oncology
  • Molecular Biology

Background:

  • Programmed death-1 (PD-1) and its ligands (PD-Ls) are key negative regulators of immune responses.
  • Their interaction suppresses T-cell function and promotes tumor immune evasion.
  • Dysregulation of PD-1/PD-L1 signaling is implicated in various cancers.

Purpose of the Study:

  • To provide an overview of the discovery and regulatory mechanisms of PD-1 and PD-L1 in tumors.
  • To elucidate the function and signaling pathways of PD-1 and its ligands.
  • To examine the roles of PD-1/PD-L1 in tumor immune evasion and clinical treatment.

Main Methods:

  • Literature review and synthesis of existing research on PD-1/PD-L1.
  • Analysis of signaling pathways involved in PD-1-mediated T-cell inhibition.
  • Review of clinical data on PD-1/PD-L1 blockade therapies.

Main Results:

  • PD-1/PD-L1 interaction inhibits effector T cells and promotes regulatory T cells (Tregs), facilitating tumor immune escape.
  • Blockade of the PD-1/PD-L1 axis restores anti-tumor immunity by reducing Treg function and enhancing effector T-cell activity.
  • Several monoclonal antibodies targeting the PD-1/PD-L1 axis have demonstrated efficacy and received regulatory approval.

Conclusions:

  • Understanding PD-1/PD-L1 dysregulation is crucial for cancer immunotherapy.
  • Targeting the PD-1/PD-L1 pathway offers a promising strategy for enhancing anti-tumor responses.
  • Further research into the precise mechanisms of PD-1 in T-cell inhibition is warranted.

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