Evidence map›Paper›PMID 30003150›Full record

ArticleHeliyon2018

Suppression of T cells by mesenchymal and cardiac progenitor cells is partly mediated via extracellular vesicles.

F van den Akker, K R Vrijsen, J C Deddens, J W Buikema, M Mokry, L W van Laake, P A Doevendans, J P G Sluijter

Abstract read
In one paragraph

Article in Heliyon, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing 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

31 citing papers in PubMed.

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  14. Cardiac Cell Therapy: Insights into the Mechanisms of Tissue Repair.International journal of molecular sciences · 2021
    Review
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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

8 authors.

F van den AkkerDepartment of Cardiology, Experimental Cardiology Laboratory, University Medical Center Utrecht, The Netherlands.
K R VrijsenDepartment of Cardiology, Experimental Cardiology Laboratory, University Medical Center Utrecht, The Netherlands.
J C DeddensDepartment of Cardiology, Experimental Cardiology Laboratory, University Medical Center Utrecht, The Netherlands.
J W BuikemaDepartment of Cardiology, Experimental Cardiology Laboratory, University Medical Center Utrecht, The Netherlands.
M MokryDivision of Pediatrics, Wilhelmina Children's Hospital, University Medical Center Utrecht, The Netherlands.
L W van LaakeDepartment of Cardiology, Experimental Cardiology Laboratory, University Medical Center Utrecht, The Netherlands.
P A DoevendansDepartment of Cardiology, Experimental Cardiology Laboratory, University Medical Center Utrecht, The Netherlands.
J P G SluijterDepartment of Cardiology, Experimental Cardiology Laboratory, University Medical Center Utrecht, The Netherlands.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Adverse remodeling after myocardial infarction (MI) is strongly influenced by T cells. Stem cell therapy after MI, using mesenchymal stem cells (MSC) or cardiomyocyte progenitor cells (CMPC), improved cardiac function, despite low cell retention and limited differentiation. As MSC secrete many factors affecting T cell proliferation and function, we hypothesized the immune response could be affected as one of the targets of stem cell therapy. Therefore, we studied the immunosuppressive properties of human BM-MSC and CMPC and their extracellular vesicles (EVs) in co-culture with activated T cells. Proliferation of T cells, measured by carboxyfluorescein succinimidyl ester dilution, was significantly reduced in the presence of BM-MSC and CMPC. The inflammatory cytokine panel of the T cells in co-culture, measured by Luminex assay, changed, with strong downregulation of IFN-gamma and TNF-alpha. The effect on proliferation was observed in both direct cell contact and transwell co-culture systems. Transfer of conditioned medium to unrelated T cells abrogated proliferation in these cells. EVs isolated from the conditioned medium of BM-MSC and CMPC prevented T cell proliferation in a dose-dependent fashion. Progenitor cells presence induces up- and downregulation of multiple previously unreported pathways in T cells. In conclusion, both BM-MSC and CMPC have a strong capacity for

Indexed as

ImmunologyStem cell research

Identifiers

PMID30003150
PMCPMC6040605

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Registered trials

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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.