Evidence map›Paper›PMID 27211104›Full record

ArticleScientific reports2016

Interferon-γ and Tumor Necrosis Factor-α Polarize Bone Marrow Stromal Cells Uniformly to a Th1 Phenotype.

Ping Jin, Yuanlong Zhao, Hui Liu, Jinguo Chen, Jiaqiang Ren, Jianjian Jin, Davide Bedognetti, Shutong Liu, Ena Wang, Francesco Marincola and 1 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
5.2field-weighted citation impact, top 3% 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

60 citing papers in PubMed, 80 citations in OpenAlex.

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  7. In situ licensing of mesenchymal stem cell immunomodulatory function via BMP-2 induced developmental process.Proceedings of the National Academy of Sciences of the United States of America · 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

11 authors at 3 institutions in 2 countries.

Ping JinCell Processing Section, Department of Transfusion Medicine, Clinical Center, National Institutes of Health, Bethesda, Maryland 20892 USA.
Yuanlong ZhaoCell Processing Section, Department of Transfusion Medicine, Clinical Center, National Institutes of Health, Bethesda, Maryland 20892 USA.
Hui LiuCell Processing Section, Department of Transfusion Medicine, Clinical Center, National Institutes of Health, Bethesda, Maryland 20892 USA.
Jinguo ChenCenter for Human Immunology (CHI), National Institutes of Health, Bethesda, MD, 20892, USA.
Jiaqiang RenCell Processing Section, Department of Transfusion Medicine, Clinical Center, National Institutes of Health, Bethesda, Maryland 20892 USA.
Jianjian JinCell Processing Section, Department of Transfusion Medicine, Clinical Center, National Institutes of Health, Bethesda, Maryland 20892 USA.
Davide BedognettiResearch Branch, Sidra Medical and Research Center, Doha, Qatar.
Shutong LiuCell Processing Section, Department of Transfusion Medicine, Clinical Center, National Institutes of Health, Bethesda, Maryland 20892 USA.
Ena WangResearch Branch, Sidra Medical and Research Center, Doha, Qatar.
Francesco MarincolaResearch Branch, Sidra Medical and Research Center, Doha, Qatar.
David StroncekCell Processing Section, Department of Transfusion Medicine, Clinical Center, National Institutes of Health, Bethesda, Maryland 20892 USA.
National Institutes of Health Clinical Center · USSidra Medical and Research Center · QANational Institutes of Health · US

Funding

Develop novel assays for assessing cellular and gene therapiesZIACL002119 · CLC · CLINICAL CENTER · PI STRONCEK, DAVID · 2010 to 2025
$0k
6 · The paper itself

Abstract

Activated T cells polarize mesenchymal stromal cells (MSCs) to a proinflammatory Th1 phenotype which likely has an important role in amplifying the immune response in the tumor microenvironment. We investigated the role of interferon gamma (IFN-γ) and tumor necrosis factor alpha (TNF-α), two factors produced by activated T cells, in MSC polarization. Gene expression and culture supernatant analysis showed that TNF-α and IFN-γ stimulated MSCs expressed distinct sets of proinflammatory factors. The combination of IFN-γ and TNF-α was synergistic and induced a transcriptome most similar to that found in MSCs stimulated with activated T cells and similar to that found in the inflamed tumor microenvironment; a Th1 phenotype with the expression of the immunosuppressive factors IL-4, IL-10, CD274/PD-L1 and indoleamine 2,3 dioxygenase (IDO). Single cell qRT-PCR analysis showed that the combination of IFN-γ and TNF-α polarized uniformly to this phenotype. The combination of IFN-γ and TNF-α results in the synergist uniform polarization of MSCs toward a primarily Th1 phenotype. The stimulation of MSCs by IFN-γ and TNF-α released from activated tumor infiltrating T cells is likely responsible for the production of many factors that characterize the tumor microenvironment.

Indexed as

Cell PolarityCells, CulturedGene Expression ProfilingGene Expression RegulationHumansInterferon-gammaMesenchymal Stem CellsSingle-Cell AnalysisTh1 CellsTranscriptomeTumor MicroenvironmentTumor Necrosis Factor-alphaInterferon-gammaTumor Necrosis Factor-alpha

Identifiers

PMID27211104
PMCPMC4876328
OpenAlexW2403062814

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.