Evidence map›Paper›PMID 40195438›Full record

ArticleScientific reports2025

Engineered PD-L1 co-expression in PD-1 knockout and MAGE-C2-targeting TCR-T cells augments the cytotoxic efficacy toward target cancer cells.

Fangxin Zhao, Xuan Zhang, Ying Tang, Hongxin Yang, Haiting Pan, Beibei Li, Riwen An, Wu Geyemuri, Chao Yang, Fang Wan and 1 more

Abstract read
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Fangxin Zhao *School of Life Sciences, Inner Mongolia University, Hohhot, Inner Mongolia, China.
Xuan Zhang *College of Basic Medicine, Inner Mongolia Medical University, Hohhot, Inner Mongolia, China.
Ying Tang *School of Life Sciences, Inner Mongolia University, Hohhot, Inner Mongolia, China.
Hongxin YangCollege of Basic Medicine, Inner Mongolia Medical University, Hohhot, Inner Mongolia, China.
Haiting PanCollege of Basic Medicine, Inner Mongolia Medical University, Hohhot, Inner Mongolia, China.
Beibei LiCollege of Basic Medicine, Inner Mongolia Medical University, Hohhot, Inner Mongolia, China.
Riwen AnCollege of Basic Medicine, Inner Mongolia Medical University, Hohhot, Inner Mongolia, China.
Wu GeyemuriCollege of Basic Medicine, Inner Mongolia Medical University, Hohhot, Inner Mongolia, China.
Chao YangCollege of Basic Medicine, Inner Mongolia Medical University, Hohhot, Inner Mongolia, China.
Fang WanSchool of Life Sciences, Inner Mongolia Agricultural University, Hohhot, Inner Mongolia, China.
Jianqiang WuSchool of Life Sciences, Inner Mongolia University, Hohhot, Inner Mongolia, China. jianqiangwu@immu.edu.cn.

Funding

Inner Mongolia Science & Technology Project Plan 2019-GG037Natural Science Research Funds of Inner Mongolia 2022MS08009
6 · The paper itself

Abstract

Expression of the PD-1 protein by tumor cells is relatively common and has been shown to exert proliferation-inhibitory effects across various tumor types, including T-cell malignancies, non-small cell lung cancer, and colon cancer. However, harnessing this tumor suppressor pathway is challenging because PD-1 activation by PD-L1 also suppresses normal T-cell function. We hypothesized that cancer antigen-specific TCR-T cells engineered to express PD-L1 could selectively activate the PD-1 pathway in tumor cells while simultaneously preventing self-inhibition by knocking out intrinsic PD-1 expression in TCR-T cells. To test this hypothesis, we co-expressed a MAGE-C2-specific recombinant TCR and the PD-L1-encoding CD274 gene in normal human T cells in which the PDCD1 gene was knocked out. These engineered TCR-T cells targeted MAGE-C2-expressing malignant cells, activating PD-1 signaling to suppress tumor proliferation while maintaining suppressed PD-1 signaling in the TCR-T cells themselves. To evaluate the tumor-suppressive potential of this approach, we compared the efficacy of PDL1-MC2-TCR-T

Indexed as

Antigens, NeoplasmB7-H1 AntigenNeoplasm ProteinsNeoplasmsProgrammed Cell Death 1 ReceptorReceptors, Antigen, T-CellT-LymphocytesAnimalsCell Line, TumorCell ProliferationGene Knockout TechniquesHumansMiceXenograft Model Antitumor AssaysAntigens, NeoplasmB7-H1 AntigenCD274 protein, humanNeoplasm ProteinsPDCD1 protein, humanProgrammed Cell Death 1 ReceptorReceptors, Antigen, T-CellCancerImmunotherapyMAGE-C2PD-1/PD-L1TCR-T

Identifiers

PMID40195438
PMCPMC11976951

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.