Evidence map›Paper›PMID 35013108›Full record

ArticleCell death & disease2022

The downregulation of type I IFN signaling in G-MDSCs under tumor conditions promotes their development towards an immunosuppressive phenotype.

Yingying Sun, Xiaoqing Han, Chao Shang, Yawei Wang, Boya Xu, Shu Jiang, Yan Mo, Dake Wang, Yueshuang Ke, Xianlu Zeng

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

21 citing papers in PubMed, 23 citations in OpenAlex.

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  14. Dual roles of CD11bFrontiers in immunology · 2024
    Article
  15. Review
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  17. 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

10 authors at 2 institutions in 1 country.

Yingying SunThe Key Laboratory of Molecular Epigenetics of Ministry of Education, Institute of Genetics and Cytology, School of Life Science, Northeast Normal University, Changchun, Jilin, China.
Xiaoqing HanLaboratory of Chemical Biology, Changchun Institute of Applied Chemistry, Chinese Academy of Sciences, Changchun, Jilin, China.
Chao ShangThe Key Laboratory of Molecular Epigenetics of Ministry of Education, Institute of Genetics and Cytology, School of Life Science, Northeast Normal University, Changchun, Jilin, China.
Yawei WangThe Key Laboratory of Molecular Epigenetics of Ministry of Education, Institute of Genetics and Cytology, School of Life Science, Northeast Normal University, Changchun, Jilin, China.
Boya XuThe Key Laboratory of Molecular Epigenetics of Ministry of Education, Institute of Genetics and Cytology, School of Life Science, Northeast Normal University, Changchun, Jilin, China.
Shu JiangThe Key Laboratory of Molecular Epigenetics of Ministry of Education, Institute of Genetics and Cytology, School of Life Science, Northeast Normal University, Changchun, Jilin, China.
Yan MoThe Key Laboratory of Molecular Epigenetics of Ministry of Education, Institute of Genetics and Cytology, School of Life Science, Northeast Normal University, Changchun, Jilin, China.
Dake WangThe Key Laboratory of Molecular Epigenetics of Ministry of Education, Institute of Genetics and Cytology, School of Life Science, Northeast Normal University, Changchun, Jilin, China.
Yueshuang KeThe Key Laboratory of Molecular Epigenetics of Ministry of Education, Institute of Genetics and Cytology, School of Life Science, Northeast Normal University, Changchun, Jilin, China. keys585@nenu.edu.cn.ORCID http://orcid.org/0000-0003-1518-4271
Xianlu ZengThe Key Laboratory of Molecular Epigenetics of Ministry of Education, Institute of Genetics and Cytology, School of Life Science, Northeast Normal University, Changchun, Jilin, China. zengx779@nenu.edu.cn.ORCID http://orcid.org/0000-0002-2655-4197
Northeast Normal University · CNChinese Academy of Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumors modify myeloid cell differentiation and induce an immunosuppressive microenvironment. Granulocytic myeloid-derived suppressor cells (G-MDSCs), the main subgroup of myeloid-derived suppressor cells (MDSCs), are immature myeloid cells (IMCs) with immunosuppressive activity and exist in tumor-bearing hosts. The reason why these cells diverge from a normal differentiation pathway and are shaped into immunosuppressive cells remains unclear. Here, we reported that the increase of granulocyte colony-stimulating factor (G-CSF) in mouse serum with tumor progression encouraged G-MDSCs to obtain immunosuppressive traits in peripheral blood through the PI3K-Akt/mTOR pathway. Importantly, we found that downregulation of type I interferon (IFN-I) signaling in G-MDSCs was a prerequisite for their immunosuppressive effects. Suppressor of cytokine signaling (SOCS1), the action of which is dependent on IFN-I signaling, inhibited the activation of the PI3K-Akt/mTOR pathway by directly interacting with Akt, indicating that the differentiation of immunosuppressive G-MDSCs involves a transition from immune activation to immune tolerance. Our study suggests that increasing IFN-I signaling in G-MDSCs may be a strategy for reprograming immunosuppressive myelopoiesis and slowing tumor progression.

Indexed as

Immune ToleranceAnimalsDisease ProgressionGranulocyte Colony-Stimulating FactorInterferon Type IMiceMyeloid-Derived Suppressor CellsMyelopoiesisNeoplasmsPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktSignal TransductionSuppressor of Cytokine Signaling 1 ProteinTOR Serine-Threonine KinasesTumor EscapeTumor MicroenvironmentGranulocyte Colony-Stimulating FactorInterferon Type IPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktSuppressor of Cytokine Signaling 1 ProteinTOR Serine-Threonine Kinases

Identifiers

PMID35013108
PMCPMC8748997
OpenAlexW4206073294

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.