Evidence map›Paper›PMID 24810636›Full record

ArticleEuropean journal of immunology2014

IFN-γ regulates survival and function of tumor-induced CD11b+ Gr-1high myeloid derived suppressor cells by modulating the anti-apoptotic molecule Bcl2a1.

José Medina-Echeverz, Lydia A Haile, Fei Zhao, Jaba Gamrekelashvili, Chi Ma, Jean-Yves Métais, Cynthia E Dunbar, Veena Kapoor, Michael P Manns, Firouzeh Korangy and 1 more

Open access · greenAbstract read
In one paragraph

Article in European journal of immunology, 2014. 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
2.3field-weighted citation impact, top 12% 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, 66 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
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  5. [Myeloid-derived suppressor cells as important factors and potential targets for breast cancer progression].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2024
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Th1-Dominant CD4Frontiers in immunology · 2022
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. 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

11 authors at 5 institutions in 2 countries.

José Medina-EcheverzGI-Malignancy Section, Thoracic and GI-Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
Lydia A Haile
Fei Zhao
Jaba Gamrekelashvili
Chi Ma
Jean-Yves Métais
Cynthia E Dunbar
Veena Kapoor
Michael P Manns
Firouzeh Korangy
Tim F Greten
Center for Cancer Research · USNational Institutes of Health · USMedizinische Hochschule Hannover · DENational Heart Lung and Blood Institute · USNational Institutes of Health Clinical Center · US

Funding

Optimization of gene transfer safety and efficacy focusing on the NHP modelZIAHL002339 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI DUNBAR, CYNTHIA E · 2009 to 2025
$26.8M
Analysis of myeloid derived suppressor cells in miceZIABC011345 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI GRETEN, TIM · 2010 to 2025
$19.5M
Intramural NIH HHS ZIA BC011345
6 · The paper itself

Abstract

Myeloid derived suppressor cells (MDSCs) play a critical role in suppression of immune responses in cancer and inflammation. Here, we describe how regulation of Bcl2a1 by cytokines controls the suppressor function of CD11b(+) Gr-1(high) granulocytic MDSCs. Coculture of CD11b(+) Gr-1(high) granulocytic MDSCs with antigen-stimulated T cells and simultaneous blockade of IFN-γ by the use of anti-IFN-γ blocking antibody, IFN-γ(-/-) effector T cells, IFN-γR(-/-) MDSCs or STAT1(-/-) MDSCs led to upregulation of Bcl2a1 in CD11b(+) Gr-1(high) cells, improved survival, and enhanced their suppressor function. Molecular studies revealed that GM-CSF released by antigen-stimulated CD8(+) T cells induced Bcl2a1 upregulation, which was repressed in the presence of IFN-γ by a direct interaction of phosphorylated STAT-1 with the Bcl2a1 promotor. Bcl2a1 overexpressing granulocytic MDSCs demonstrated prolonged survival and enhanced suppressor function in vitro. Our data suggest that IFN-γ/ STAT1-dependent regulation of Bcl2a1 regulates survival and thereby suppressor function of granulocytic MDSCs.

Indexed as

AnimalsApoptosisCD11b AntigenCD8-Positive T-LymphocytesCell LineFemaleGranulocyte-Macrophage Colony-Stimulating FactorInterferon-gammaMiceMice, Inbred BALB CMice, Inbred C57BLMinor Histocompatibility AntigensMyeloid CellsProto-Oncogene Proteins c-bcl-2Receptors, ChemokineSTAT1 Transcription FactorBCL2-related protein A1CD11b AntigenGr-1 protein, mouseGranulocyte-Macrophage Colony-Stimulating FactorInterferon-gammaMinor Histocompatibility AntigensProto-Oncogene Proteins c-bcl-2Receptors, ChemokineStat1 protein, mouseSTAT1 Transcription FactorBcl2a1GM-CSFG-MDSCIFN-γImmunotherapyVaccine

Identifiers

PMID24810636
PMCPMC4140991
OpenAlexW1921318307

What OpenQuestion holds

Textmetadata
LicenceTDM
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.