Evidence map›Paper›PMID 25400932›Full record

ArticleImmunity, inflammation and disease2014

Myeloid suppressor cells require membrane TNFR2 expression for suppressive activity.

Johannes Polz, Annika Remke, Sabine Weber, Dominic Schmidt, Dorothea Weber-Steffens, Anne Pietryga-Krieger, Nils Müller, Uwe Ritter, Sven Mostböck, Daniela N Männel

Open access · goldAbstract read
In one paragraph

Article in Immunity, inflammation and disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed, 2 pooled it
2.8field-weighted citation impact, top 9% 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

64 citing papers in PubMed, 2 syntheses or guidelines pooled it, 98 citations in OpenAlex.

  1. Pooled it
  2. TNFRSF1B Is Associated with ANCA in IBD.Inflammatory bowel diseases · 2016
    Pooled it
  3. Review
  4. Article
  5. Article
  6. Review
  7. In situ blockade of TNF-TNFR2 axis via oncolytic adenovirus improves antitumor efficacy in solid tumors.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Deletion of the non-adjacent genesFrontiers in immunology · 2023
    Article
  17. Review
  18. Review
  19. Article
  20. Review

4 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

10 authors at 2 institutions in 2 countries.

Johannes PolzInstitute of Immunology, University of Regensburg Regensburg, Germany.
Annika RemkeInstitute of Immunology, University of Regensburg Regensburg, Germany.
Sabine WeberInstitute of Immunology, University of Regensburg Regensburg, Germany.
Dominic SchmidtInstitute of Immunology, University of Regensburg Regensburg, Germany.
Dorothea Weber-SteffensInstitute of Immunology, University of Regensburg Regensburg, Germany.
Anne Pietryga-KriegerInstitute of Immunology, University of Regensburg Regensburg, Germany.
Nils MüllerInstitute of Immunology, University of Regensburg Regensburg, Germany.
Uwe RitterInstitute of Immunology, University of Regensburg Regensburg, Germany.
Sven MostböckInstitute of Immunology, University of Regensburg Regensburg, Germany.
Daniela N MännelInstitute of Immunology, University of Regensburg Regensburg, Germany.
University of Regensburg · DEInstitute of Immunology · HR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

TNF and TNF receptor type 2 (TNFR2) have been shown to be important for generation of myeloid-derived suppressor cells (MDSC). In order to analyze whether and how TNFR2 passes the effect of TNF on, myeloid cells from TNFR2-deficient mice were compared to respective cells from wild-type mice. Primary TNFR2-deficient myeloid cells showed reduced production of NO and IL-6 which was attributable to CD11b(+) CD11c(-) Ly6C(+) Ly6G(-) immature monocytic MDSC. TNFR2-deficient MDSC isolated from bone marrow were less suppressive for T cell proliferation compared to WT-derived MDSC. These differences on myeloid cells between the two mouse lines were still observed after co-culture of bone marrow cells from the two mouse lines together during myeloid cell differentiation, which demonstrated that the impaired functional capacity of TNFR2-deficient cells was independent of soluble factors but required membrane expression of TNFR2. Similarly, adoptive transfer of TNFR2-deficient bone marrow cells into wild-type hosts did not rescue the TNFR2-specific phenotype of bone marrow-derived myeloid cells. Therefore, membrane TNFR2 expression determines generation and function of monocytic MDSC.

Indexed as

Immune suppressioninflammationtumor necrosis factor

Identifiers

PMID25400932
PMCPMC4217546
OpenAlexW1508172388

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.