Evidence map›Paper›PMID 40966452›Full record

ArticleStem cells translational medicine2025

Anti-tumor effect of intratumoral administration of induced pluripotent stem cell-derived NKT cells on glioblastoma through CD155/DNAM-1 interaction.

Ko Ozaki, Takahiro Aoki, Masayoshi Kobayashi, Mariko Takami, Midori Kobayashi, Toshihiro Ito, Keita Ogawa, Hidekazu Tanaka, Kai Nishii, Katsuhiro Nishimura and 10 more

Abstract read
In one paragraph

Article in Stem cells translational medicine, 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
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  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

20 authors.

Ko OzakiDepartment of Medical Immunology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan.ORCID 0000-0003-1619-7824
Takahiro AokiDepartment of Medical Immunology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan.
Masayoshi KobayashiDepartment of Medical Immunology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan.
Mariko TakamiDepartment of Medical Immunology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan.
Midori KobayashiDepartment of Medical Immunology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan.
Toshihiro ItoDepartment of Medical Immunology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan.
Keita OgawaDepartment of Medical Immunology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan.
Hidekazu TanakaDepartment of Medical Immunology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan.
Kai NishiiDepartment of Medical Immunology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan.
Katsuhiro NishimuraDepartment of Medical Immunology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan.
Kiwamu MotoyoshiDepartment of Medical Immunology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan.
Iori KojimaDepartment of Medical Immunology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan.
Daisuke KatsumiDepartment of Medical Immunology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan.
Daiki ShimizuDepartment of Medical Immunology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan.
Hongxuan WangDepartment of Medical Immunology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan.
Motoko Yagi KimuraDepartment of Experimental Immunology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan.
Kiyoshi HiraharaDepartment of Immunology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan.
Haruhiko KosekiLaboratory for Developmental Genetics, RIKEN Center for Integrative Medical Sciences, Yokohama 230-0045, Japan.
Yoshinori HiguchiDepartment of Neurological Surgery, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan.
Shinichiro MotohashiDepartment of Medical Immunology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan.ORCID 0000-0002-9332-3129

Funding

BrightPath Biotherapeutics Co. LtdJapan Society for the Promotion of Science 20K17917Japan Society for the Promotion of Science 22H03182Japan Society for the Promotion of Science 24K19541
6 · The paper itself

Abstract

backgroundGlioblastoma is the most malignant brain tumor with the poorest prognosis, but there have been no significant therapeutic advances in the past 20 years. Intratumoral administration of invariant natural killer T (iNKT) cells for glioblastoma has recently been reported and is promising immunotherapy. However, the low presence of iNKT cells in peripheral blood made it difficult to use iNKT cells as adoptive immunotherapy. Therefore, we used induced pluripotent stem cell-derived NKT (iPS-NKT) cells and analyzed their anti-tumor effect.

methodsInduced pluripotent stem cell-derived NKT cells were generated by the previously reported protocol. The anti-tumor effect of iPS-NKT cells was confirmed against several glioblastoma cell lines. We also analyzed the expression of natural killer cell receptors of iPS-NKT cells and ligands of glioblastoma cell lines to know which interactions are dominant. In vivo, using an orthotopic glioblastoma mouse model, we compared the survival and tumor volume in mice iPS-NKT cells administered intratumorally with those in mice of no treatment group.

resultsWe demonstrated that iPS-NKT cells have anti-tumor effects even in glioma cell lines with low CD1d expression and that CD155/DNAM-1 interactions are associated with these anti-tumor effects. In the orthotopic low CD1d-expressing glioblastoma mouse model, iPS-NKT-treated mice showed markedly prolonged survival and suppressed tumor volume.

conclusionWe confirmed the anti-tumor effects of iPS-NKT cells on glioblastoma cells in vitro and in vivo. The anti-tumor activity was suggested to be mainly due to the interaction between CD155 and DNAM-1. Intratumoral administration of iPS-NKT cells has potential anti-tumor effects on glioblastoma in the clinic.

Indexed as

Brain NeoplasmsGlioblastomaInduced Pluripotent Stem CellsNatural Killer T-CellsReceptors, VirusAnimalsCell Line, TumorHumansImmunotherapy, AdoptiveMiceT Lineage-Specific Activation Antigen 1Xenograft Model Antitumor Assayspoliovirus receptorReceptors, VirusT Lineage-Specific Activation Antigen 1cancer immunotherapyCD155glioblastomaiPS cellsNK cell receptorNKT cells

Identifiers

PMID40966452
PMCPMC12445658

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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.