Evidence map›Paper›PMID 27322208›Full record

ArticleOncotarget2016

TGF-β1 contributes to CD8+ Treg induction through p38 MAPK signaling in ovarian cancer microenvironment.

Meng Wu, Xian Chen, Jianfang Lou, Shuping Zhang, Xiaojie Zhang, Lei Huang, Ruihong Sun, Peijun Huang, Fang Wang, Shiyang Pan

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.4field-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

32 citing papers in PubMed, 40 citations in OpenAlex.

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  6. Circulating CD4Medicina (Kaunas, Lithuania) · 2023
    Article
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  20. Cell-mediated immune resistance in cancer.Cancer drug resistance (Alhambra, Calif.) · 2020
    Article
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

10 authors at 3 institutions in 1 country.

Meng WuDepartment of Laboratory Medicine, The First Affiliated Hospital of Nanjing Medical University, 210029, Nanjing, China.
Xian ChenDepartment of Laboratory Medicine, The First Affiliated Hospital of Nanjing Medical University, 210029, Nanjing, China.
Jianfang LouDepartment of Laboratory Medicine, The First Affiliated Hospital of Nanjing Medical University, 210029, Nanjing, China.
Shuping ZhangDepartment of Laboratory Medicine, The Affiliated Children Hospital, Nanjing Medical University, 210029, Nanjing, China.
Xiaojie ZhangDepartment of Laboratory Medicine, The First Affiliated Hospital of Nanjing Medical University, 210029, Nanjing, China.
Lei HuangDepartment of Laboratory Medicine, The First Affiliated Hospital of Nanjing Medical University, 210029, Nanjing, China.
Ruihong SunDepartment of Laboratory Medicine, The First Affiliated Hospital of Nanjing Medical University, 210029, Nanjing, China.
Peijun HuangDepartment of Laboratory Medicine, The First Affiliated Hospital of Nanjing Medical University, 210029, Nanjing, China.
Fang WangDepartment of Laboratory Medicine, The First Affiliated Hospital of Nanjing Medical University, 210029, Nanjing, China.
Shiyang PanDepartment of Laboratory Medicine, The First Affiliated Hospital of Nanjing Medical University, 210029, Nanjing, China.
Nanjing Medical University · CNNanjing University · CNJiangsu Province Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CD8+ regulatory T cells (Tregs) contribute to cancer progression and immune evasion. We previously reported that CD8+ Tregs could be induced in vitro by co-culture of CD8+ T cells with the OC cell lines SKOV3/A2780. Here, we described the role of TGF-β1 in CD8+ Treg induction by the OC microenvironment. OC patients expressed high levels of TGF-β1, as did the co-culture supernatant from CD8+ T cells and SKOV3. Additionally, TGF-β1 levels were positively correlated with CD8+ Treg percentages in OC. Neutralization experiments, cytokine studies and proliferation assays revealed that the in vitro-induced CD8+Tregs depended at least partially on up-regulated expression of TGF-β1 to exert their suppressive function. CD8+ T cells cultured with SKOV3 exhibited marked activation of p38 MAPK than CD8+ T cells cultured alone, which could be inhibited by TGF-β1-neutralizing antibody. Moreover, the p38 specific inhibitor SB203580 dose-dependently blocked the TGF-β1 activated conversion of CD8+ T cells into CD8+ Tregs. These data suggested that in vitro-induction of CD8+ Tregs depended in part on TGF-β1 activation of p38 MAPK signaling. Therefore, p38 MAPK could be a therapeutic target in OC anti-tumor immunotherapy.

Indexed as

AdultAgedCD8 AntigensCD8-Positive T-LymphocytesCell Line, TumorCells, CulturedCoculture TechniquesEnzyme InhibitorsFemaleHumansImidazolesMAP Kinase Signaling SystemMiddle AgedOvarian Neoplasmsp38 Mitogen-Activated Protein KinasesPyridinesCD8 AntigensEnzyme InhibitorsImidazolesp38 Mitogen-Activated Protein KinasesPyridinesSB 203580Transforming Growth Factor beta1CD8+ Tregovarian cancerp38 MAPKTGF-β1

Identifiers

PMID27322208
PMCPMC5190116
OpenAlexW2427429764

What OpenQuestion holds

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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.