Evidence map›Paper›PMID 40277917›Full record

ArticleCells2025

Regulatory T Cell Mimicry by a Subset of Mesenchymal GBM Stem Cells Suppresses CD4 and CD8 Cells.

Amanda L Johnson, Harmon S Khela, Jack Korleski, Sophie Sall, Yunqing Li, Weiqiang Zhou, Karen Smith-Connor, John Laterra, Hernando Lopez-Bertoni

Abstract read
In one paragraph

Article in Cells, 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. Article
  4. CD39Frontiers in oncology · 2025
    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

9 authors.

Amanda L JohnsonHugo W. Moser Research Institute at Kennedy Krieger, Baltimore, MD 21205, USA.ORCID 0000-0002-3055-945X
Harmon S KhelaHugo W. Moser Research Institute at Kennedy Krieger, Baltimore, MD 21205, USA.
Jack KorleskiHugo W. Moser Research Institute at Kennedy Krieger, Baltimore, MD 21205, USA.ORCID 0000-0003-3845-7869
Sophie SallHugo W. Moser Research Institute at Kennedy Krieger, Baltimore, MD 21205, USA.ORCID 0009-0001-4234-4077
Yunqing LiHugo W. Moser Research Institute at Kennedy Krieger, Baltimore, MD 21205, USA.ORCID 0000-0002-9679-505X
Weiqiang ZhouDepartment of Biostatistics, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD 21205, USA.ORCID 0000-0001-9396-9571
Karen Smith-ConnorHugo W. Moser Research Institute at Kennedy Krieger, Baltimore, MD 21205, USA.
John LaterraHugo W. Moser Research Institute at Kennedy Krieger, Baltimore, MD 21205, USA.
Hernando Lopez-BertoniHugo W. Moser Research Institute at Kennedy Krieger, Baltimore, MD 21205, USA.ORCID 0000-0001-6618-1092

Funding

Translational Research Central ServicesP30CA006973 · NCI · JOHNS HOPKINS UNIVERSITY · PI ALAN KEITH MEEKER · 1985 to 2026
$208.6M
Sleep and Circadian Dysfunction, Brain and Neurobehavioral Development in AutismP50HD103538 · NICHD · HUGO W. MOSER RES INST KENNEDY KRIEGER · PI Stewart H Mostofsky · 2020 to 2026
$9.9M
Chromatin Modifications in GBM-Propagating CellsR01NS096754 · NINDS · HUGO W. MOSER RES INST KENNEDY KRIEGER · PI LATERRA, JOHN J · 2017 to 2021
$2.2M
Molecular determinants of cellular heterogeneity and therapeutic resistance in GBM.R01NS120949 · NINDS · HUGO W. MOSER RES INST KENNEDY KRIEGER · PI LOPEZ-BERTONI, HERNANDO MARTIN · 2021 to 2025
$2.0M
Dissecting the tumor cell-immune TME axis to identify therapeutically actionable vulnerabilities that potentiate immunotherapy in GBMF99CA284254 · NCI · JOHNS HOPKINS UNIVERSITY · PI JOHNSON, AMANDA · 2023 to 2024
$98k
NCI NIH HHS F99 CA284254NCI NIH HHS F99CA284254NCI NIH HHS P30 CA006973NCI NIH HHS P30CA006973NICHD NIH HHS P50 HD103538NIH HHS 1R01NS120949-06A1NINDS NIH HHS R01 NS096754NINDS NIH HHS R01NS096754NINDS NIH HHS R01 NS120949
6 · The paper itself

Abstract

Attempts to activate an anti-tumor immune response in glioblastoma (GBM) have been met with many challenges due to its inherently immunosuppressive tumor microenvironment. The degree and mechanisms by which molecularly and phenotypically diverse tumor-propagating glioma stem cells (GSCs) contribute to this state are poorly defined. In this study, our multifaceted approach combining bioinformatics analyses of clinical and experimental datasets, single-cell sequencing, and the molecular and pharmacologic manipulation of patient-derived cells identified GSCs expressing immunosuppressive effectors mimicking regulatory T cells (Tregs). We showed that this immunosuppressive Treg-like (ITL) GSC state is specific to the mesenchymal GSC subset and is associated with and driven specifically by TGFβ type II receptor (TGFBR2) in contrast to TGFBR1. Transgenic TGFBR2 expression in patient-derived GBM neurospheres promoted a mesenchymal transition and induced a six-gene ITL signature consisting of

Indexed as

Brain NeoplasmsCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesGlioblastomaMesenchymal Stem CellsNeoplastic Stem CellsT-Lymphocytes, RegulatoryAnimalsCell Line, TumorHumansReceptor, Transforming Growth Factor-beta Type IITumor MicroenvironmentReceptor, Transforming Growth Factor-beta Type IITGFBR2 protein, humanGBMGSCimmunosuppressionTGFBR2

Identifiers

PMID40277917
PMCPMC12026101

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.