Evidence map›Paper›PMID 37770968›Full record

ArticleJournal of translational medicine2023

B7H3-targeting chimeric antigen receptor modification enhances antitumor effect of Vγ9Vδ2 T cells in glioblastoma.

Yi Wang, Nan Ji, Yang Zhang, Junsheng Chu, Changcun Pan, Peng Zhang, Weiwei Ma, Xueguang Zhang, Jianzhong Jeff Xi, Mingze Chen and 3 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.7field-weighted citation impact, top 6% of its field
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

17 citing papers in PubMed, 16 citations in OpenAlex.

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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

13 authors at 5 institutions in 2 countries.

Yi WangBeijing Advanced Innovation Center for Biomedical Engineering, Beijing Advanced Innovation Center for Big Data-Based Precision Medicine, Beihang University, Beijing, 100191, China.
Nan JiBeijing Advanced Innovation Center for Biomedical Engineering, Beijing Advanced Innovation Center for Big Data-Based Precision Medicine, Beihang University, Beijing, 100191, China.
Yang ZhangDepartment of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100070, China.
Junsheng ChuDepartment of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100070, China.
Changcun PanDepartment of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100070, China.
Peng ZhangDepartment of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100070, China.
Weiwei MaTsinghua-Peking Center for Life Sciences, State Key Laboratory of Membrane Biology, School of Pharmaceutical Sciences, Tsinghua University, Beijing, 100084, China.
Xueguang ZhangJiangsu Institute of Clinical Immunology, First Affiliated Hospital, Jiangsu Provincial Key Laboratory of Stem Cell and Biomedical Materials, Soochow University, Soochow University, Suzhou, 215000, China.
Jianzhong Jeff XiState Key Laboratory of Natural and Biomimetic Drugs, Institute of Molecular Medicine, Department of Biomedical Engineering, College of Engineering, Peking University, Beijing, 100871, China.
Mingze ChenDepartment of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100070, China.
Yonghui ZhangTsinghua-Peking Center for Life Sciences, State Key Laboratory of Membrane Biology, School of Pharmaceutical Sciences, Tsinghua University, Beijing, 100084, China. zhangyonghui@tsinghua.edu.cn.
Liwei ZhangBeijing Advanced Innovation Center for Biomedical Engineering, Beijing Advanced Innovation Center for Big Data-Based Precision Medicine, Beihang University, Beijing, 100191, China. zhanglw@bjtth.org.
Tao SunDepartment of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100070, China. suntao@bjtth.org.ORCID http://orcid.org/0009-0003-4678-1981
Capital Medical University · CNBeijing Tian Tan Hospital · CNCenter for Life Sciences · CNPeking University · CNSoochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGlioblastoma (GBM) is a highly aggressive primary brain tumor with a poor prognosis. This study investigates the therapeutic potential of human Vγ9Vδ2 T cells in GBM treatment. The sensitivity of different glioma specimens to Vγ9Vδ2 T cell-mediated cytotoxicity is assessed using a patient-derived tumor cell clusters (PTCs) model.

methodsThe study evaluates the anti-tumor effect of Vγ9Vδ2 T cells in 26 glioma cases through the PTCs model. Protein expression of BTN2A1 and BTN3A1, along with gene expression related to lipid metabolism and glioma inflammatory response pathways, is analyzed in matched tumor tissue samples. Additionally, the study explores two strategies to re-sensitize tumors in the weak anti-tumor effect (WAT) group: utilizing a BTN3A1 agonistic antibody or employing bisphosphonates to inhibit farnesyl diphosphate synthase (FPPS). Furthermore, the study investigates the efficacy of genetically engineered Vγ9Vδ2 T cells expressing Car-B7H3 in targeting diverse GBM specimens.

resultsThe results demonstrate that Vγ9Vδ2 T cells display a stronger anti-tumor effect (SAT) in six glioma cases, while showing a weaker effect (WAT) in twenty cases. The SAT group exhibits elevated protein expression of BTN2A1 and BTN3A1, accompanied by differential gene expression related to lipid metabolism and glioma inflammatory response pathways. Importantly, the study reveals that the WAT group GBM can enhance Vγ9Vδ2 T cell-mediated killing sensitivity by incorporating either a BTN3A1 agonistic antibody or bisphosphonates. Both approaches support TCR-BTN mediated tumor recognition, which is distinct from the conventional MHC-peptide recognition by αβ T cells. Furthermore, the study explores an alternative strategy by genetically engineering Vγ9Vδ2 T cells with Car-B7H3, and both non-engineered and Car-B7H3 Vγ9Vδ2 T cells demonstrate promising efficacy in vivo, underscoring the versatile potential of Vγ9Vδ2 T cells for GBM treatment.

conclusionsVγ9Vδ2 T cells demonstrate a robust anti-tumor effect in some glioma cases, while weaker in others. Elevated BTN2A1 and BTN3A1 expression correlates with improved response. WAT group tumors can be sensitized using a BTN3A1 agonistic antibody or bisphosphonates. Genetically engineered Vγ9Vδ2 T cells, i.e.,  Car-B7H3, show promising efficacy. These results together highlight the versatility of Vγ9Vδ2 T cells for GBM treatment.

Indexed as

GlioblastomaReceptors, Chimeric AntigenAntigens, CDButyrophilinsDiphosphonatesHumansReceptors, Antigen, T-Cell, gamma-deltaT-LymphocytesAntigens, CDBTN3A1 protein, humanButyrophilinsDiphosphonatesReceptors, Antigen, T-Cell, gamma-deltaReceptors, Chimeric AntigenB7-H3BTN2A1BTN3A1GlioblastomaVγ9Vδ2 T cells

Identifiers

PMID37770968
PMCPMC10537973
OpenAlexW4387119939

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.