Evidence map›Paper›PMID 30194424›Full record

ArticleScientific reports2018

Genetic screen in myeloid cells identifies TNF-α autocrine secretion as a factor increasing MDSC suppressive activity via Nos2 up-regulation.

Matthias Schröder, Marit Krötschel, Lena Conrad, Svenja Kerstin Naumann, Christopher Bachran, Alex Rolfe, Viktor Umansky, Laura Helming, Lee Kim Swee

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 26% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Schlafen4Frontiers in immunology · 2023
    Article
  9. Review
  10. CD8British journal of cancer · 2021
    Article
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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

9 authors at 4 institutions in 2 countries.

Matthias SchröderBioMed X Innovation Center, Heidelberg, Germany.ORCID 0000-0002-6603-9851
Marit KrötschelBioMed X Innovation Center, Heidelberg, Germany.
Lena ConradBioMed X Innovation Center, Heidelberg, Germany.
Svenja Kerstin NaumannBioMed X Innovation Center, Heidelberg, Germany.
Christopher BachranBioMed X Innovation Center, Heidelberg, Germany.
Alex RolfeEMD Serono, Billerica, USA.
Viktor UmanskySkin Cancer Unit, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Laura HelmingMerck KGaA, Darmstadt, Germany.
Lee Kim SweeBioMed X Innovation Center, Heidelberg, Germany. swee@bio.mx.
BioMed X Institute · DEGerman Cancer Research Center · DEMerck (Germany) · DEOno Pharmaceutical (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The suppressive microenvironment of tumors remains one of the limiting factors for immunotherapies. In tumors, the function of effector T cells can be inhibited by cancer cells as well as myeloid cells including tumor associated macrophages and myeloid-derived suppressor cells (MDSC). A better understanding of how myeloid cells inhibit T cell function will guide the design of therapeutic strategies to increase anti-tumor responses. We have previously reported the in vitro differentiation of MDSC from immortalized mouse hematopoietic progenitors and characterized the impact of retinoic acid and 3-deazaneplanocin A on MDSC development and function. We describe here the effect of these compounds on MDSC transcriptome and identify genes and pathway affected by the treatment. In order to accelerate the investigation of gene function in MDSC suppressive activity, we developed protocols for CRISPR/Cas9-mediated gene editing in MDSC. Through screening of 217 genes, we found that autocrine secretion of TNF-α contributes to MDSC immunosuppressive activity through up-regulation of Nos2. The approach described here affords the investigation of gene function in myeloid cells such as MDSC with unprecedented ease and throughput.

Indexed as

Autocrine CommunicationAnimalsCells, CulturedCRISPR-Cas SystemsGene EditingMiceMice, Inbred C57BLMyeloid-Derived Suppressor CellsNitric Oxide Synthase Type IITranscriptomeTumor Necrosis Factor-alphaUp-RegulationNitric Oxide Synthase Type IINos2 protein, mouseTumor Necrosis Factor-alpha

Identifiers

PMID30194424
PMCPMC6128861
OpenAlexW2891099107

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.