Evidence map›Paper›PMID 18453563›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2008

Cutting edge: expression of TNFR2 defines a maximally suppressive subset of mouse CD4+CD25+FoxP3+ T regulatory cells: applicability to tumor-infiltrating T regulatory cells.

Xin Chen, Jeffrey J Subleski, Heather Kopf, O M Zack Howard, Daniela N Männel, Joost J Oppenheim

Open access · greenAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 193 papers.

0numbers the graph read from it
0cells of the map it votes in
193citing papers in PubMed
5.6field-weighted citation impact, top 3% 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

193 citing papers in PubMed, 320 citations in OpenAlex.

  1. Article
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  4. Decoding TNF receptor superfamily control of CD4Cell communication and signaling : CCS · 2026
    Review
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  13. Circulating Inflammation Biomarkers and the Risk of Esophageal Adenocarcinoma: A Nested Case-Control Study in the Department of Defense Serum Repository.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2025
    Article
  14. Article
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  17. Understanding the role of TNFR2 signaling in the tumor microenvironment of breast cancer.Journal of experimental & clinical cancer research : CR · 2024
    Review
  18. Article
  19. Review
  20. Review

133 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

6 authors at 4 institutions in 2 countries.

Xin ChenBasic Research Program, SAIC-Frederick Inc, National Cancer Institute (NCI)-Frederick, Frederick, MD 21702-1201, USA. chenxin@mail.nih.gov
Jeffrey J Subleski
Heather Kopf
O M Zack Howard
Daniela N Männel
Joost J Oppenheim
Frederick National Laboratory for Cancer Research · USCancer Research Center · USScience Applications International Corporation (United States) · USUniversity of Regensburg · DE

Funding

SEA Influenza Clinical Research NetworkN01CO12400 · NCI · LEIDOS BIOMEDICAL RESEARCH, INC. · 2007 to 2008
$225.2M
Studies of Receptor Interactions and Effects of AlarminsZIABC009369 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI OPPENHEIM, JOOST J · 2009 to 2022
$16.5M
Role of T regulatory suppression in autoimmunity and cancerZ01BC010707 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI OPPENHEIM, JOOST J · 2006 to 2008
$755k
Intramural NIH HHS Z01 BC010707Intramural NIH HHS Z99 CA999999NCI NIH HHS N01 CO012400NCI NIH HHS N01 CO 12400
6 · The paper itself

Abstract

TNFR2 is predominantly expressed by a subset of human and mouse CD4(+)CD25(+)FoxP3(+) T regulatory cells (Tregs). In this study, we characterized the phenotype and function of TNFR2(+) Tregs in peripheral lymphoid tissues of normal and tumor-bearing C57BL/6 mice. We found that TNFR2 was expressed on 30-40% of the Tregs of the peripheral activated/memory subset that were most highly suppressive. In contrast, TNFR2(-) Tregs exhibited the phenotype of naive cells and only had minimal suppressive activity. Although not typically considered to be Tregs, CD4(+)CD25(-)TNFR2(+) cells nevertheless possessed moderate suppressive activity. Strikingly, the suppressive activity of TNFR2(+) Tregs was considerably more potent than that of reportedly highly suppressive CD103(+) Tregs. In the Lewis lung carcinoma model, more highly suppressive TNFR2(+) Tregs accumulated intratumorally than in the periphery. Thus, TNFR2 identifies a unique subset of mouse Tregs with an activated/memory phenotype and maximal suppressive activity that may account for tumor-infiltrating lymphocyte-mediated immune evasion by tumors.

Indexed as

AnimalsCarcinoma, Lewis LungCD4 AntigensFemaleFlow CytometryForkhead Transcription FactorsInterleukin-2 Receptor alpha SubunitLymphocyte ActivationLymphocytes, Tumor-InfiltratingMiceMice, Inbred C57BLPhenotypeReceptors, Tumor Necrosis Factor, Type IIT-Lymphocytes, RegulatoryT-Lymphocyte SubsetsTumor EscapeCD4 AntigensForkhead Transcription FactorsFoxp3 protein, mouseInterleukin-2 Receptor alpha SubunitReceptors, Tumor Necrosis Factor, Type II

Identifiers

PMID18453563
PMCPMC2699949
OpenAlexW2162124617

What OpenQuestion holds

Textmetadata
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.