Evidence map›Paper›PMID 32911844›Full record

ArticleCells2020

Impact of Bone Marrow miR-21 Expression on Acute Myeloid Leukemia T Lymphocyte Fragility and Dysfunction.

Douâa Moussa Agha, Redouane Rouas, Mehdi Najar, Fatima Bouhtit, Hussein Fayyad-Kazan, Laurence Lagneaux, Dominique Bron, Nathalie Meuleman, Philippe Lewalle, Makram Merimi

Open access · goldAbstract read
In one paragraph

Article in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

13 citing papers in PubMed, 21 citations in OpenAlex.

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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

10 authors at 3 institutions in 4 countries.

Douâa Moussa AghaLaboratory of Experimental Hematology, Jules Bordet Institute, Université Libre de Bruxelles, 1000 Bruxelles, Belgium.
Redouane RouasLaboratory of Experimental Hematology, Jules Bordet Institute, Université Libre de Bruxelles, 1000 Bruxelles, Belgium.
Mehdi NajarOsteoarthritis Research Unit, University of Montreal Hospital Research Center (CRCHUM) and Department of Medicine, University of Montreal, Montreal, QC H2X 0A9, Canada.ORCID 0000-0002-9740-9122
Fatima BouhtitLaboratory of Experimental Hematology, Jules Bordet Institute, Université Libre de Bruxelles, 1000 Bruxelles, Belgium.
Hussein Fayyad-KazanLaboratory of Cancer Biology and Molecular Immunology, Faculty of Sciences I, Lebanese University, Hadath 90656, Lebanon.
Laurence LagneauxLaboratory of Clinical Cell Therapy, Jules Bordet Institute, Université Libre de Bruxelles, 1070 Bruxelles, Belgium.
Dominique BronLaboratory of Experimental Hematology, Jules Bordet Institute, Université Libre de Bruxelles, 1000 Bruxelles, Belgium.
Nathalie MeulemanLaboratory of Experimental Hematology, Jules Bordet Institute, Université Libre de Bruxelles, 1000 Bruxelles, Belgium.
Philippe LewalleLaboratory of Experimental Hematology, Jules Bordet Institute, Université Libre de Bruxelles, 1000 Bruxelles, Belgium.
Makram MerimiLaboratory of Experimental Hematology, Jules Bordet Institute, Université Libre de Bruxelles, 1000 Bruxelles, Belgium.
Université Libre de Bruxelles · BELebanese University · LBMohamed I University · MA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAcute myeloid leukemia (AML) is a hematopoietic malignancy in which antitumor immunity is impaired. The therapeutic management of AML requires understanding the mechanisms involved in the fragility and immune dysfunction of AML T lymphocytes.

methodsIn this study, T lymphocytes from healthy donors (HD) and AML patients were used. Extracellular vesicles (EVs) from leukemic cells were screened for their microRNA content and impact on T lymphocytes. Flow cytometry, transcriptomic as well as lentiviral transduction techniques were used to carry out the research.

resultsWe observed increased cell death of T lymphocytes from AML patients. EVs from leukemia myeloid cell lines harbored several miRNAs, including miR-21, and were able to induce T lymphocyte death. Compared to that in HD, miR-21 was overexpressed in both the bone marrow fluid and infiltrating T lymphocytes of AML patients. MiR-21 induces T lymphocyte cell death by upregulating proapoptotic gene expression. It also increases the immunosuppressive profile of T lymphocytes by upregulating the IL13, IL4, IL10, and FoxP3 genes.

conclusionsOur results demonstrate that miR-21 plays a significant role in AML T lymphocyte dysfunction and apoptosis. Targeting miR-21 may be a novel approach to restore the efficacy of the immune response against AML.

Indexed as

ApoptosisBone MarrowCase-Control StudiesFemaleHumansInterleukinsLeukemia, Myeloid, AcuteMaleMicroRNAsMiddle AgedT-LymphocytesInterleukinsMicroRNAsMIRN21 microRNA, humanAMLapoptosisextracellular vesiclesimmunosuppressionmiR21T lymphocytes

Identifiers

PMID32911844
PMCPMC7563595
OpenAlexW3084281103

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.