ArticlePloS one2013
Engineered drug resistant γδ T cells kill glioblastoma cell lines during a chemotherapy challenge: a strategy for combining chemo- and immunotherapy.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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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.
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.
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Who cites it
63 citing papers in PubMed, 85 citations in OpenAlex.
- Review
- Harnessing the potential of γδ T cells through engineering and combination treatment for cancer therapies.Nature communications · 2026Review
- Targeting NKG2D/NKG2DL axis in cancer immunotherapy: mechanisms and therapeutic applications.Journal of translational medicine · 2026Review
- Cell therapies against brain tumors: Clinical development and emerging prospects.Bioengineering & translational medicine · 2025Review
- Review
- Article
- Article
- Arming Vδ2 T Cells with Chimeric Antigen Receptors to Combat Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024Review
- Targeting NKG2D ligands in glioblastoma with a bispecific T-cell engager is augmented with conventional therapy and enhances oncolytic virotherapy of glioma stem-like cells.Journal for immunotherapy of cancer · 2024Article
- Evolution of cell therapy for renal cell carcinoma.Molecular cancer · 2024Review
- Controversial role of γδ T cells in colorectal cancer.American journal of cancer research · 2024Review
- Directing the migration of serum-free,Frontiers in immunology · 2024Article
- Adoptive cell therapy for high grade gliomas using simultaneous temozolomide and intracranial mgmt-modified γδ t cells following standard post-resection chemotherapy and radiotherapy: current strategy and future directions.Frontiers in immunology · 2024Article
- Review
- γδ T cells: origin and fate, subsets, diseases and immunotherapy.Signal transduction and targeted therapy · 2023Review
- Classification and function of γδT cells and its research progress in anti-glioblastoma.Discover oncology · 2023Review
- An immunosuppressed microenvironment distinguishes lateral ventricle-contacting glioblastomas.JCI insight · 2023Article
- Enhancing the effectiveness of γδ T cells by mRNA transfection of chimeric antigen receptors or bispecific T cell engagers.Molecular therapy oncolytics · 2023Article
- γδ T cells as a potential therapeutic agent for glioblastoma.Frontiers in immunology · 2023Review
- Vγ9Vδ2 T-cell immunotherapy in blood cancers: ready for prime time?Frontiers in immunology · 2023Review
3 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Classical approaches to immunotherapy that show promise in some malignancies have generally been disappointing when applied to high-grade brain tumors such as glioblastoma multiforme (GBM). We recently showed that ex vivo expanded/activated γδ T cells recognize NKG2D ligands expressed on malignant glioma and are cytotoxic to glioma cell lines and primary GBM explants. In addition, γδ T cells extend survival and slow tumor progression when administered to immunodeficient mice with intracranial human glioma xenografts. We now show that temozolomide (TMZ), a principal chemotherapeutic agent used to treat GBM, increases the expression of stress-associated NKG2D ligands on TMZ-resistant glioma cells, potentially rendering them vulnerable to γδ T cell recognition and lysis. TMZ is also highly toxic to γδ T cells, however, and to overcome this cytotoxic effect γδ T cells were genetically modified using a lentiviral vector encoding the DNA repair enzyme O(6)-alkylguanine DNA alkyltransferase (AGT) from the O(6)-methylguanine methyltransferase (MGMT) cDNA, which confers resistance to TMZ. Genetic modification of γδ T cells did not alter their phenotype or their cytotoxicity against GBM target cells. Importantly, gene modified γδ T cells showed greater cytotoxicity to two TMZ resistant GBM cell lines, U373(TMZ-R) and SNB-19(TMZ-R) cells, in the presence of TMZ than unmodified cells, suggesting that TMZ exposed more receptors for γδ T cell-targeted lysis. Therefore, TMZ resistant γδ T cells can be generated without impairing their anti-tumor functions in the presence of high concentrations of TMZ. These results provide a mechanistic basis for combining chemotherapy and γδ T cell-based drug resistant cellular immunotherapy to treat GBM.
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Registered trials
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.