Evidence map›Paper›PMID 26321145›Full record

ArticleStem cell reports2015

Interleukin-25 Mediates Transcriptional Control of PD-L1 via STAT3 in Multipotent Human Mesenchymal Stromal Cells (hMSCs) to Suppress Th17 Responses.

Wei-Bei Wang, Men-Luh Yen, Ko-Jiunn Liu, Pei-Ju Hsu, Ming-Hong Lin, Pei-Min Chen, Putty-Reddy Sudhir, Chein-Hung Chen, Chung-Hsuan Chen, Huei-Kang Sytwu and 1 more

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

Article in Stem cell reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

41 citing papers in PubMed, 77 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

11 authors at 5 institutions in 1 country.

Wei-Bei WangRegenerative Medicine Research Group, Institute of Cellular & System Medicine, National Health Research Institutes (NHRI), Zhunan 35053, Taiwan.
Men-Luh YenDepartment of Obstetrics/Gynecology, National Taiwan University Hospital and School of Medicine, College of Medicine, National Taiwan University, Taipei 10051, Taiwan.
Ko-Jiunn LiuNational Institute of Cancer Research, NHRI, Tainan 70403, Taiwan; Taipei Medical University, Taipei 10031, Taiwan. Electronic address: kojiunn@nhri.org.tw.
Pei-Ju HsuRegenerative Medicine Research Group, Institute of Cellular & System Medicine, National Health Research Institutes (NHRI), Zhunan 35053, Taiwan.
Ming-Hong LinGraduate Institute of Immunology, National Defense Medical Center, Taipei 11490, Taiwan.
Pei-Min ChenDepartment of Obstetrics/Gynecology, National Taiwan University Hospital and School of Medicine, College of Medicine, National Taiwan University, Taipei 10051, Taiwan.
Putty-Reddy SudhirGenomic Research Center, Academia Sinica, Taipei 11529, Taiwan.
Chein-Hung ChenGenomic Research Center, Academia Sinica, Taipei 11529, Taiwan.
Chung-Hsuan ChenGenomic Research Center, Academia Sinica, Taipei 11529, Taiwan.
Huei-Kang SytwuGraduate Institute of Immunology, National Defense Medical Center, Taipei 11490, Taiwan.
B Linju YenRegenerative Medicine Research Group, Institute of Cellular & System Medicine, National Health Research Institutes (NHRI), Zhunan 35053, Taiwan; Department of Obstetrics/Gynecology, Cathay General Hospital Shiji, Taipei 21174, Taiwan. Electronic address: blyen@nhri.org.tw.
Genomics Research Center, Academia Sinica · TWNational Health Research Institutes · TWNational Defense Medical Center · TWNational Taiwan University Hospital · TWTaipei Medical University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multipotent human mesenchymal stromal cells (hMSCs) harbor immunomodulatory properties that are therapeutically relevant. One of the most clinically important populations of leukocytes is the interleukin-17A (IL-17A)-secreting T (Th17) lymphocytes. However, mechanisms of hMSC and Th17 cell interactions are incompletely resolved. We found that, along with Th1 responses, hMSCs strongly suppressed Th17 responses and this required both IL-25--also known as IL--17E-as well as programmed death ligand-1 (PD-L1), a potent cell surface ligand for tolerance induction. Knockdown of IL-25 expression in hMSCs abrogated Th17 suppression in vitro and in vivo. However, IL-25 alone was insufficient to significantly suppress Th17 responses, which also required surface PD-L1 expression. Critically, IL-25 upregulated PD-L1 surface expression through the signaling pathways of JNK and STAT3, with STAT3 found to constitutively occupy the proximal region of the PD-L1 promoter. Our findings demonstrate the complexities of hMSC-mediated Th17 suppression, and highlight the IL-25/STAT3/PD-L1 axis as a candidate therapeutic target.

Indexed as

B7-H1 AntigenGene Expression RegulationGene Knockdown TechniquesHumansInterleukin-17Mesenchymal Stem CellsSTAT3 Transcription FactorTh17 CellsTranscription, GeneticB7-H1 AntigenCD274 protein, humanIL25 protein, humanInterleukin-17STAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID26321145
PMCPMC4618596
OpenAlexW1915829159

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.