Evidence map›Paper›PMID 40076788›Full record

ArticleInternational journal of molecular sciences2025

Unusual Partners: γδ-TCR-Based T Cell Therapy in Combination with Oncolytic Virus Treatment for Diffuse Midline Gliomas.

Konstantinos Vazaios, Patricia Hernández López, Tineke Aarts-Riemens, Annet Daudeij, Vera Kemp, Rob C Hoeben, Trudy Straetemans, Esther Hulleman, Friso G Calkoen, Jasper van der Lugt and 1 more

Abstract read
In one paragraph

Article in International journal of molecular sciences, 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.

Konstantinos VazaiosPrincess Máxima Center for Pediatric Oncology, 3584 CS Utrecht, The Netherlands.ORCID 0000-0002-3623-0348
Patricia Hernández LópezCenter for Translational Immunology, University Medical Center Utrecht, Utrecht University, 3584 CX Utrecht, The Netherlands.
Tineke Aarts-RiemensCenter for Translational Immunology, University Medical Center Utrecht, Utrecht University, 3584 CX Utrecht, The Netherlands.
Annet DaudeijCenter for Translational Immunology, University Medical Center Utrecht, Utrecht University, 3584 CX Utrecht, The Netherlands.
Vera KempDepartment of Cell and Chemical Biology, Leiden University Medical Center, Leiden University, 2333 ZC Leiden, The Netherlands.ORCID 0000-0003-4910-4655
Rob C HoebenDepartment of Cell and Chemical Biology, Leiden University Medical Center, Leiden University, 2333 ZC Leiden, The Netherlands.ORCID 0000-0001-9443-8377
Trudy StraetemansCenter for Translational Immunology, University Medical Center Utrecht, Utrecht University, 3584 CX Utrecht, The Netherlands.
Esther HullemanPrincess Máxima Center for Pediatric Oncology, 3584 CS Utrecht, The Netherlands.ORCID 0000-0001-9256-947X
Friso G CalkoenPrincess Máxima Center for Pediatric Oncology, 3584 CS Utrecht, The Netherlands.ORCID 0000-0001-9059-0929
Jasper van der LugtPrincess Máxima Center for Pediatric Oncology, 3584 CS Utrecht, The Netherlands.ORCID 0000-0002-8186-338X
Jürgen KuballCenter for Translational Immunology, University Medical Center Utrecht, Utrecht University, 3584 CX Utrecht, The Netherlands.ORCID 0000-0002-3914-7806

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Due to the minimal survival benefits of existing therapies for pediatric diffuse midline glioma (DMG) patients, new therapeutic modalities are being investigated. Immunotherapies such as CAR-T cells and oncolytic viruses (OVs) are part of these efforts, as evidenced by the increasing number of clinical trials. αβ T cells engineered with a high-affinity γ9δ2 T-cell receptor (TEGs) are immune cells designed to target metabolic changes in malignant or virally infected cells via BTN2A1 and BTN3A. Because the expression of BTN2A1 and BTN3A can be altered in tumor and infected cells, combining TEGs and OVs could potentially enhance the anti-tumor response. We investigated this hypothesis in the following study. We demonstrate that TEGs can indeed target DMG, which expresses BTN2A1 and BTN3A at varying levels, and that OVs can further enhance the expression of BTN3A-but not BTN2A1-in DMG. Functionally, TEGs killed DMG cell cultures, and this killing was further increased after OV infection of the DMGs with either adenovirus Δ24-RGD or reovirus R124 under suboptimal conditions. However, this additive effect was lost when γ9δ2 TCR-ligand interaction was boosted by pamidronate. This study demonstrates the additive effect of combining OVs and Vγ9Vδ2 TCR-engineered immune cells under suboptimal conditions and supports a combination strategy to enhance the efficacy of both therapeutic modalities.

Indexed as

Brain NeoplasmsGliomaImmunotherapy, AdoptiveOncolytic VirotherapyOncolytic VirusesReceptors, Antigen, T-Cell, gamma-deltaT-LymphocytesCell Line, TumorCombined Modality TherapyHumansReceptors, Antigen, T-Cell, gamma-delta?9?2TCRD24-RGDdiffuse midline gliomaimmune-oncologyimmunotherapyoncolytic virusesR124TEGs

Identifiers

PMID40076788
PMCPMC11900589

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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.