Evidence map›Paper›PMID 24259296›Full record

ArticleInternational journal of cancer2014

Subpopulations of myeloid-derived suppressor cells impair T cell responses through independent nitric oxide-related pathways.

Patrick L Raber, Paul Thevenot, Rosa Sierra, Dorota Wyczechowska, Daniel Halle, Maria E Ramirez, Augusto C Ochoa, Matthew Fletcher, Cruz Velasco, Anna Wilk and 2 more

Abstract read
In one paragraph

Article in International journal of cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 187 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
187citing papers in PubMed, 1 pooled it
5.7field-weighted citation impact, top 4% 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

187 citing papers in PubMed, 1 synthesis or guideline pooled it, 288 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. CD13 identifies S100A4Biology direct · 2026
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  17. Myeloid-derived suppressor cells modulation in the context of tumor microenvironment for gastric cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Review
  18. Article
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  20. Article

127 more citing papers are in PubMed but not listed here.

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

12 authors at 1 institution in 1 country.

Patrick L RaberDepartment of Microbiology, Immunology, and Parasitology, Louisiana State University Health Sciences Center, New Orleans, LA; Stanley S. Scott Cancer Center, Louisiana State University Health Sciences Center, New Orleans, LA.
Paul Thevenot
Rosa Sierra
Dorota Wyczechowska
Daniel Halle
Maria E Ramirez
Augusto C Ochoa
Matthew Fletcher
Cruz Velasco
Anna Wilk
Krzysztof Reiss
Paulo C Rodriguez
Louisiana State University Health Sciences Center New Orleans · US

Funding

TUMOR MICROENVIRONMENT AND B CELL LYMPHOMASP20RR021970 · NCRR · LSU HEALTH SCIENCES CENTER · PI THOMPSON, HILARY W · 2005 to 2011
$14.1M
Mentoring Translational Researchers in LouisianaP20GM103501 · NIGMS · LSU HEALTH SCIENCES CENTER · PI OCHOA, AUGUSTO C. · 2012 to 2014
$6.3M
Metabolic approaches to treat severe viral and inflammatory diseasesR01AI112402 · NIAID · LSU HEALTH SCIENCES CENTER · PI OCHOA, AUGUSTO C. · 2013 to 2017
$2.6M
Notch-1 in T Cells: a central mediator of tumor induced anergyR21CA162133 · NCI · LSU HEALTH SCIENCES CENTER · PI RODRIGUEZ, PAULO CESAR · 2012 to 2013
$330k
NCI NIH HHS NIH-R21CA162133NCI NIH HHS R21 CA162133NCRR NIH HHS P20 RR021970NIAID NIH HHS R01 AI112402NIGMS NIH HHS P20 GM103501NIGMS NIH HHS P20GM103501
6 · The paper itself

Abstract

The accumulation of myeloid-derived suppressor cells (MDSC) in tumor-bearing hosts is a hallmark of malignancy-associated inflammation and a major mediator for the induction of T cell suppression in cancer. MDSC can be divided phenotypically into granulocytic (G-MDSC) and monocytic (Mo-MDSC) subgroups. Several mechanisms mediate the induction of T cell anergy by MDSC; however, the specific role of these pathways in the inhibitory activity of MDSC subpopulations remains unclear. Therefore, we aimed to determine the effector mechanisms by which subsets of tumor-infiltrating MDSC block T cell function. We found that G-MDSC had a higher ability to impair proliferation and expression of effector molecules in activated T cells, as compared to Mo-MDSC. Interestingly, both MDSC subgroups inhibited T cells through nitric oxide (NO)-related pathways, but expressed different effector inhibitory mechanisms. Specifically, G-MDSC impaired T cells through the production of peroxynitrites (PNT), while Mo-MDSC suppressed by the release of NO. The production of PNT in G-MDSC depended on the expression of gp91(phox) and endothelial NO synthase (eNOS), while inducible NO synthase (iNOS) mediated the generation of NO in Mo-MDSC. Deletion of eNOS and gp91(phox) or scavenging of PNT blocked the suppressive function of G-MDSC and induced anti-tumoral effects, without altering Mo-MDSC inhibitory activity. Furthermore, NO-scavenging or iNOS knockdown prevented Mo-MDSC function, but did not affect PNT production or suppression by G-MDSC. These results suggest that MDSC subpopulations utilize independent effector mechanisms to regulate T cell function. Inhibition of these pathways is expected to specifically block MDSC subsets and overcome immune suppression in cancer.

Indexed as

AnimalsCD8-Positive T-LymphocytesCell Line, TumorCell ProliferationFemaleGranulocytesHumansLymphocyte ActivationMembrane GlycoproteinsMiceMice, Inbred C57BLMonocytesNADPH Oxidase 2NADPH OxidasesNeoplasmsNitric OxideCybb protein, mouseMembrane GlycoproteinsNADPH Oxidase 2NADPH OxidasesNitric OxideNitric Oxide Synthase Type IINitric Oxide Synthase Type IIINitritesNos2 protein, mouseNos3 protein, mousePeroxynitrous AcidReactive Oxygen SpecieseNOSMDSCperoxynitrites

Identifiers

PMID24259296
PMCPMC3980009
OpenAlexW1552212814

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.