Evidence map›Paper›PMID 28781075›Full record

ArticleStem cell reports2017

Activated Tissue-Resident Mesenchymal Stromal Cells Regulate Natural Killer Cell Immune and Tissue-Regenerative Function.

Robert Michael Petri, Alexander Hackel, Katrin Hahnel, Claudia Alexandra Dumitru, Kirsten Bruderek, Stefanie B Flohe, Annette Paschen, Stephan Lang, Sven Brandau

Open access · goldAbstract read
In one paragraph

Article in Stem cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

59 citing papers in PubMed, 93 citations in OpenAlex.

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  11. The Effect of Mesenchymal Stem Cells on the Wound Infection.Current stem cell research & therapy · 2024
    Review
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  14. Advances in Stem Cell-Based Therapies in the Treatment of Osteoarthritis.International journal of molecular sciences · 2023
    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

9 authors at 1 institution in 1 country.

Robert Michael PetriDepartment of Otorhinolaryngology, University Hospital Essen, University of Duisburg-Essen, Essen 45147, Germany.
Alexander HackelDepartment of Otorhinolaryngology, University Hospital Essen, University of Duisburg-Essen, Essen 45147, Germany.
Katrin HahnelDepartment of Otorhinolaryngology, University Hospital Essen, University of Duisburg-Essen, Essen 45147, Germany.
Claudia Alexandra DumitruDepartment of Otorhinolaryngology, University Hospital Essen, University of Duisburg-Essen, Essen 45147, Germany.
Kirsten BruderekDepartment of Otorhinolaryngology, University Hospital Essen, University of Duisburg-Essen, Essen 45147, Germany.
Stefanie B FloheDepartment of Orthopedics and Trauma Surgery, University Hospital Essen, University of Duisburg-Essen, Essen 45147, Germany.
Annette PaschenDepartment of Dermatology, University Hospital Essen, University of Duisburg-Essen, Essen 45147, Germany.
Stephan LangDepartment of Otorhinolaryngology, University Hospital Essen, University of Duisburg-Essen, Essen 45147, Germany.
Sven BrandauDepartment of Otorhinolaryngology, University Hospital Essen, University of Duisburg-Essen, Essen 45147, Germany. Electronic address: sven.brandau@uk-essen.de.
University of Duisburg-Essen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The interaction of mesenchymal stromal cells (MSCs) with natural killer (NK) cells is traditionally thought of as a static inhibitory model, whereby resting MSCs inhibit NK cell effector function. Here, we use a dynamic in vitro system of poly(I:C) stimulation to model the interaction of NK cells and tissue-resident MSCs in the context of infection or tissue injury. The experiments suggest a time-dependent system of regulation and feedback, where, at early time points, activated MSCs secrete type I interferon to enhance NK cell effector function, while at later time points TGF-β and IL-6 limit NK cell effector function and terminate inflammatory responses by induction of a regulatory senescent-like NK cell phenotype. Importantly, feedback of these regulatory NK cells to MSCs promotes survival, proliferation, and pro-angiogenic properties. Our data provide additional insight into the interaction of stromal cells and innate immune cells and suggest a model of time-dependent MSC polarization and licensing.

Indexed as

RegenerationApoptosisBone Marrow CellsCell CommunicationCell DifferentiationCell ProliferationCell SurvivalCellular SenescenceCytotoxicity, ImmunologicHumansInflammationInterleukin-6Killer Cells, NaturalLymphocyte ActivationMesenchymal Stem CellsNasal MucosaInterleukin-6Poly I-CReceptors, CXCR4Transforming Growth Factor betamesenchymal stromal cell polarizationmucosal tissuenatural killer cell activationPoly(I:C)senescenceTGF-βTLR 3type I interferonviral infection

Identifiers

PMID28781075
PMCPMC5599186
OpenAlexW2744021789

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.