Evidence map›Paper›PMID 28287112›Full record

ArticleCellular & molecular immunology2018

Glucocorticoid receptor promotes the function of myeloid-derived suppressor cells by suppressing HIF1α-dependent glycolysis.

Yun Lu, Huanrong Liu, Yujing Bi, Hui Yang, Yan Li, Jian Wang, Zhengguo Zhang, Yu Wang, Chunxiao Li, Anna Jia and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Cellular & molecular immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

47 citing papers in PubMed, 76 citations in OpenAlex.

  1. Review
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  5. Myeloid metabolism and its role in immunotherapy of cancer.Journal for immunotherapy of cancer · 2025
    Review
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  9. Review
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  16. Article
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  18. Article
  19. Review
  20. Metabolites as drivers and targets in rheumatoid arthritis.Clinical and experimental immunology · 2022
    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

15 authors at 5 institutions in 2 countries.

Yun LuDepartment of Immunology, School of Basic Medical Sciences, Fudan University, 200032, Shanghai, China.
Huanrong LiuDepartment of Immunology, School of Basic Medical Sciences, Fudan University, 200032, Shanghai, China.
Yujing BiState Key laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology, 100071, Beijing, China.
Hui YangDepartment of Immunology, School of Basic Medical Sciences, Fudan University, 200032, Shanghai, China.
Yan LiDepartment of Immunology, School of Basic Medical Sciences, Fudan University, 200032, Shanghai, China.
Jian WangDepartment of Immunology, School of Basic Medical Sciences, Fudan University, 200032, Shanghai, China.
Zhengguo ZhangDepartment of Immunology, School of Basic Medical Sciences, Fudan University, 200032, Shanghai, China.
Yu WangDepartment of Immunology, School of Basic Medical Sciences, Fudan University, 200032, Shanghai, China.
Chunxiao LiDepartment of Immunology, School of Basic Medical Sciences, Fudan University, 200032, Shanghai, China.
Anna JiaKey Laboratory of Cell Proliferation and Regulation Biology of Ministry of Education, Institute of Cell Biology, College of Life Sciences, Beijing Normal University, 100875, Beijing, China.
Linian HanKey Laboratory of Cell Proliferation and Regulation Biology of Ministry of Education, Institute of Cell Biology, College of Life Sciences, Beijing Normal University, 100875, Beijing, China.
Ying HuKey Laboratory of Cell Proliferation and Regulation Biology of Ministry of Education, Institute of Cell Biology, College of Life Sciences, Beijing Normal University, 100875, Beijing, China.
Yong ZhaoState Key Laboratory of Membrane Biology, Institute of Zoology, Chinese Academy of Sciences, 100101, Beijing, China. zhaoy@ioz.ac.cn.
Ruoning WangCenter for Childhood Cancer and Blood Diseases, Hematology/Oncology and BMT, The Research Institute at Nationwide Children's Hospital, Ohio State University, 43205, Columbus, USA, Ohio. zhaoy@ioz.ac.cn.
Guangwei LiuDepartment of Immunology, School of Basic Medical Sciences, Fudan University, 200032, Shanghai, China. zhaoy@ioz.ac.cn.
Beijing Normal University · CNShanghai Medical College of Fudan University · CNChinese Academy of Sciences · CNInstitute of Microbiology · CNNationwide Children's Hospital · US

Funding

Metabolic programming in TH17 cell differentiationR01AI114581 · NIAID · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI WANG, RUONING · 2015 to 2025
$3.6M
Metabolic dysregulation and therapeutic intervention in asthmaR21AI117547 · NIAID · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI WANG, RUONING, ZHANG, JIAN · 2015 to 2016
$428k
NIAID NIH HHS R01 AI114581NIAID NIH HHS R21 AI117547
6 · The paper itself

Abstract

Immunomodulatory signaling imposes tight regulations on metabolic programs within immune cells and consequentially determines immune response outcomes. Although the glucocorticoid receptor (GR) has been recently implicated in regulating the function of myeloid-derived suppressor cells (MDSCs), whether the dysregulation of GR in MDSCs is involved in immune-mediated hepatic diseases and how GR regulates the function of MDSCs in such a context remains unknown. Here, we revealed the dysregulation of GR expression in MDSCs during innate immunological hepatic injury (IMH) and found that GR regulates the function of MDSCs through modulating HIF1α-dependent glycolysis. Pharmacological modulation of GR by its agonist (dexamethasone, Dex) protects IMH mice against inflammatory injury. Mechanistically, GR signaling suppresses HIF1α and HIF1α-dependent glycolysis in MDSCs and thus promotes the immune suppressive activity of MDSCs. Our studies reveal a role of GR-HIF1α in regulating the metabolism and function of MDSCs and further implicate MDSC GR signaling as a potential therapeutic target in hepatic diseases that are driven by innate immune cell-mediated systemic inflammation.

Indexed as

GlycolysisAnimalsDexamethasoneDisease Models, AnimalDown-RegulationHumansHypoxia-Inducible Factor 1, alpha SubunitImmune ToleranceImmunity, InnateInflammationLipopolysaccharidesLiverMice, Inbred C57BLMifepristoneMyeloid-Derived Suppressor CellsReceptors, GlucocorticoidDexamethasoneHypoxia-Inducible Factor 1, alpha SubunitLipopolysaccharidesMifepristoneReceptors, Glucocorticoid

Identifiers

PMID28287112
PMCPMC6079089
OpenAlexW2596861603

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.