Evidence map›Paper›PMID 28002798›Full record

ArticleOncotarget2017

IL-17A weakens the antitumor immuity by inhibiting apoptosis of MDSCs in Lewis lung carcinoma bearing mice.

Juan Wang, Yue Zhang, Kai Yin, Peiqi Xu, Jie Tian, Jie Ma, Xinyu Tian, Yungang Wang, Xinyi Tang, Huaxi Xu and 1 more

Erratum issuedOpen access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.8field-weighted citation impact, top 27% 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

9 citing papers in PubMed, 19 citations in OpenAlex.

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  9. Mechanisms and Applications of γδ T Cells in Anti-Tumor Immunity.Cancer control : journal of the Moffitt Cancer Center
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 1 country.

Juan WangDepartment of Laboratory Medicine, The Affiliated People's Hospital, Jiangsu University, Zhenjiang, China.
Yue ZhangDepartment of Laboratory Medicine, The Affiliated People's Hospital, Jiangsu University, Zhenjiang, China.
Kai YinDepartment of General Surgery, The Affiliated Hospital, Jiangsu University, Zhenjiang, China.
Peiqi XuInstitute of Laboratory Medicine, Jiangsu Key Laboratory of Laboratory Medicine, School of Medicine, Jiangsu University, Zhenjiang, China.
Jie TianInstitute of Laboratory Medicine, Jiangsu Key Laboratory of Laboratory Medicine, School of Medicine, Jiangsu University, Zhenjiang, China.
Jie MaInstitute of Laboratory Medicine, Jiangsu Key Laboratory of Laboratory Medicine, School of Medicine, Jiangsu University, Zhenjiang, China.
Xinyu TianInstitute of Laboratory Medicine, Jiangsu Key Laboratory of Laboratory Medicine, School of Medicine, Jiangsu University, Zhenjiang, China.
Yungang WangInstitute of Laboratory Medicine, Jiangsu Key Laboratory of Laboratory Medicine, School of Medicine, Jiangsu University, Zhenjiang, China.
Xinyi TangInstitute of Laboratory Medicine, Jiangsu Key Laboratory of Laboratory Medicine, School of Medicine, Jiangsu University, Zhenjiang, China.
Huaxi XuInstitute of Laboratory Medicine, Jiangsu Key Laboratory of Laboratory Medicine, School of Medicine, Jiangsu University, Zhenjiang, China.
Shengjun WangDepartment of Laboratory Medicine, The Affiliated People's Hospital, Jiangsu University, Zhenjiang, China.
Jiangsu University · CNAffiliated Hospital of Jiangsu University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myeloid-derived suppressor cells (MDSCs) weaken the antitumor immune response through the inhibition of effector T cell activity and the production of immunosuppressive factors in pathological sites. It is well established that interleukin-17A (IL-17A) has a remarkable role on the promotion of inflammation and tumor formation, and IL-17 has been implicated in the enhancement of immunosuppression of MDSCs, which consequently promotes tumor progression. A detailed study of this relationship remains elusive. In our study, we not only confirmed the promotion of IL-17 on Lewis lung carcinoma (LLC) development but also surprisingly showed that IL-17 could extend the fate and enhance the immunosuppressive effect of MDSCs through activating ERK1/2. Additionally, the effect of IL-17 on MDSCs was reversed, even in tumors by blocking ERK1/2. Interdicting the signaling molecule ERK1/2 could increase the apoptosis of MDSCs and weaken the suppressive activity of MDSCs, so that thereafter, the antitumor immunity could be restored partly. Therefore, these findings offer new insights into the importance of IL-17 and the downstream signaling factor ERK1/2 for MDSCs.

Indexed as

AnimalsApoptosisCarcinoma, Lewis LungCell Line, TumorInjections, SubcutaneousInterleukin-17MAP Kinase Signaling SystemMiceMyeloid-Derived Suppressor CellsIl17a protein, mouseInterleukin-17apoptosisinterleukin-17myeloid-derived suppressor cellstumor immunology

Identifiers

PMID28002798
PMCPMC5354873
OpenAlexW2561205642

What OpenQuestion holds

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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.