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Updated: Mar 10, 2026

Identifying PD-1/PD-L1 Inhibitors with Surface Plasmon Resonance Technology
Published on: May 2, 2025
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.
Abstract:
Checkpoint programmed death-1 (PD-1)/programmed cell death ligands (PD-Ls) have been identified as negative immunoregulatory molecules that promote immune evasion of tumor cells. The interaction of PD-1 and PD-Ls inhibits the function of T cells and tumor-infiltrating lymphocytes (TIL) while increasing the function of immunosuppressive regulatory T cells (Tregs). This condition causes the tumor cells to evade immune response. Thus, the blockade of PD-1/PD-L1 enhances anti-tumor immunity by reducing the number and/or the suppressive activity of Tregs and by restoring the activity of effector T cells. Furthermore, some monoclonal antibodies blockading PD-1/PD-Ls axis have achieved good effect and received Food and Drug Administration approval. The role of PD-1/PD-Ls in tumors has been well studied, but little is known on the mechanism by which PD-1 blocks T-cell activation. In this study, we provide a brief overview on the discovery and regulatory mechanism of PD-1 and PD-L1 dysregulation in tumors, as well as the function and signaling pathway of PD-1 and its ligands; their roles in tumor evasion and clinical treatment were also studied.
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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