Evidence map›Paper›PMID 34727093›Full record

ArticleJCI insight2021

Tnfrsf4-expressing regulatory T cells promote immune escape of chronic myeloid leukemia stem cells.

Magdalena Hinterbrandner, Viviana Rubino, Carina Stoll, Stefan Forster, Noah Schnüriger, Ramin Radpour, Gabriela M Baerlocher, Adrian F Ochsenbein, Carsten Riether

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

28 citing papers in PubMed, 39 citations in OpenAlex.

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  13. Murine Regulatory CD4International journal of molecular sciences · 2024
    Article
  14. Prognostic Significance of Regulatory T-Cells and PD-1 + CD8 T-Cells in Chronic Myeloid Leukemia Patients Treated with Generic Imatinib.Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2024
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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

9 authors at 2 institutions in 1 country.

Magdalena HinterbrandnerDepartment of Medical Oncology, Inselspital, Bern University Hospital.
Viviana RubinoDepartment of Medical Oncology, Inselspital, Bern University Hospital.
Carina StollDepartment of Medical Oncology, Inselspital, Bern University Hospital.
Stefan ForsterDepartment of Medical Oncology, Inselspital, Bern University Hospital.
Noah SchnürigerDepartment of Medical Oncology, Inselspital, Bern University Hospital.
Ramin RadpourDepartment of Medical Oncology, Inselspital, Bern University Hospital.
Gabriela M BaerlocherDepartment for BioMedical Research (DBMR).
Adrian F OchsenbeinDepartment of Medical Oncology, Inselspital, Bern University Hospital.
Carsten RietherDepartment of Medical Oncology, Inselspital, Bern University Hospital.
University Hospital of Bern · CHUniversity of Bern · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Leukemia stem cells (LSCs) promote the disease and seem resistant to therapy and immune control. Why LSCs are selectively resistant against elimination by CD8+ cytotoxic T cells (CTLs) is still unknown. In this study, we demonstrate that LSCs in chronic myeloid leukemia (CML) can be recognized and killed by CD8+ CTLs in vitro. However, Tregs, which preferentially localized close to CD8+ CTLs in CML BM, protected LSCs from MHC class I-dependent CD8+ CTL-mediated elimination in vivo. BM Tregs in CML were characterized by the selective expression of tumor necrosis factor receptor 4 (Tnfrsf4). Stimulation of Tnfrsf4 signaling did not deplete Tregs but reduced the capacity of Tregs to protect LSCs from CD8+ CTL-mediated killing. In the BM of newly diagnosed CML patients, TNFRSF4 mRNA levels were significantly increased and correlated with the expression of the Treg-restricted transcription factor FOXP3. Overall, these results identify Tregs as key regulators of immune escape of LSCs and TNFRSF4 as a potential target to reduce the function of Tregs and boost antileukemic immunity in CML.

Indexed as

AnimalsChronic DiseaseFemaleHumansImmunotherapyLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMaleMiceReceptors, OX40T-Lymphocytes, RegulatoryTumor EscapeReceptors, OX40TNFRSF4 protein, humanCancer immunotherapyHematologyLeukemiasStem cells

Identifiers

PMID34727093
PMCPMC8675189
OpenAlexW3210665441

What OpenQuestion holds

Textmetadata
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.