Evidence map›Paper›PMID 25584044›Full record

ArticleFrontiers in immunology2014

Human Umbilical Cord-Derived Mesenchymal Stem Cells Utilize Activin-A to Suppress Interferon-γ Production by Natural Killer Cells.

Debanjana Chatterjee, Nicole Marquardt, Dejene Milkessa Tufa, Tim Hatlapatka, Ralf Hass, Cornelia Kasper, Constantin von Kaisenberg, Reinhold Ernst Schmidt, Roland Jacobs

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.3field-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

35 citing papers in PubMed, 57 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

9 authors at 2 institutions in 2 countries.

Debanjana ChatterjeeDepartment of Clinical Immunology and Rheumatology, Hannover Medical School , Hannover , Germany.
Nicole MarquardtDepartment of Clinical Immunology and Rheumatology, Hannover Medical School , Hannover , Germany.
Dejene Milkessa TufaDepartment of Clinical Immunology and Rheumatology, Hannover Medical School , Hannover , Germany.
Tim HatlapatkaInstitute of Technical Chemistry, Leibniz University of Hannover , Hannover , Germany.
Ralf HassLaboratory of Biochemistry and Tumor Biology, Clinic of Obstetrics and Gynecology, Hannover Medical School , Hannover , Germany.
Cornelia KasperInstitute of Technical Chemistry, Leibniz University of Hannover , Hannover , Germany ; Department of Biotechnology, University of Natural Resources and Life Science , Vienna , Austria.
Constantin von KaisenbergDepartment of Obstetrics, Gynecology and Reproductive Medicine, Hannover Medical School , Hannover , Germany.
Reinhold Ernst SchmidtDepartment of Clinical Immunology and Rheumatology, Hannover Medical School , Hannover , Germany.
Roland JacobsDepartment of Clinical Immunology and Rheumatology, Hannover Medical School , Hannover , Germany.
Medizinische Hochschule Hannover · DELeibniz University Hannover · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Following allogeneic hematopoietic stem cell transplantation (HSCT), interferon (IFN)-γ levels in the recipient's body can strongly influence the clinical outcome. Human umbilical cord-derived mesenchymal stem cells (UC-MSCs) are lucrative as biological tolerance-inducers in HSCT settings. Hence, we studied the molecular mechanism of how UC-MSCs influence natural killer (NK) cell-mediated IFN-γ production. Allogeneic NK cells were cultured in direct contact with UC-MSCs or cell-free supernatants from mesenchymal stem cell (MSC) cultures (MSC-conditioned media). We found that soluble factors secreted by UC-MSCs strongly suppressed interleukin (IL)-12/IL-18-induced IFN-γ production by NK cells by reducing phosphorylation of STAT4, NF-κB, as well as T-bet activity. UC-MSCs secreted considerable amounts of activin-A, which could suppress IFN-γ production by NK cells. Neutralization of activin-A in MSC-conditioned media significantly abrogated their suppressive abilities. Till date, multiple groups have reported that prostaglandin (PG)-E2 produced by MSCs can suppress NK cell functions. Indeed, we found that inhibition of PGE2 production by MSCs could also significantly restore IFN-γ production. However, the effects of activin-A and PGE2 were not cumulative. To the best of our knowledge, we are first to report the role of activin-A in MSC-mediated suppression of IFN-γ production by NK cells.

Indexed as

activin-AIFN-γ productionNK cellsuppressionT-betUC-MSC

Identifiers

PMID25584044
PMCPMC4278046
OpenAlexW2049111133

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.