Evidence map›Paper›PMID 24213679›Full record

ReviewCancer immunology, immunotherapy : CII2014

Regulatory T cell subsets in human cancer: are they regulating for or against tumor progression?

Theresa L Whiteside

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cancer immunology, immunotherapy : CII, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
101citing papers in PubMed, 1 pooled it
11.9field-weighted citation impact, top 1% 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

101 citing papers in PubMed, 1 synthesis or guideline pooled it, 167 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
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  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Tumor-derived Exosomes and Antitumor Immunity.Journal of immunology (Baltimore, Md. : 1950) · 2024
    Review
  12. Review
  13. Review
  14. Review
  15. CD26 and Cancer.Cancers · 2022
    Article
  16. Altered mucosal immunity in HIV-positive colon adenoma: decreased CD4International journal of clinical oncology · 2022
    Article
  17. Article
  18. Article
  19. Article
  20. Review

41 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

1 author at 1 institution in 1 country.

Theresa L WhitesideDepartments of Pathology and Immunology, University of Pittsburgh Cancer Institute, University of Pittsburgh School of Medicine, 5117 Centre Avenue, Suite 1.27, Pittsburgh, PA, 15213, USA, whitesidetl@upmc.edu.
University of Pittsburgh · US

Funding

Tissue Procurement / ImmunohistologyP01CA109688 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SCHLESSELMAN, JAMES J · 2006 to 2010
$5.9M
Restoring anti-tumor immunity in the microenvironment of head and neck cancerR01CA168628 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI WHITESIDE, THERESA L. · 2013 to 2017
$1.7M
NCI NIH HHS P01 CA109688NCI NIH HHS R01 CA168628
6 · The paper itself

Abstract

Regulatory T cells (Treg) play a key role in maintaining the balance of immune responses in human health and in disease. Treg come in many flavors and can utilize a variety of mechanisms to modulate immune responses. In cancer, inducible (i) or adaptive Treg expand, accumulate in tissues and the peripheral blood of patients, and represent a functionally prominent component of CD4+ T lymphocytes. Phenotypically and functionally, iTreg are distinct from natural (n) Treg. A subset of iTreg expressing ectonucleotidases, CD39 and CD73, is able to hydrolyze ATP to 5'-AMP and adenosine (ADO) and thus mediate suppression of those immune cells which express ADO receptors. iTeg can also produce prostaglandin E2 (PGE2). These iTreg, expanding in response to tumor antigens and cytokines such as TGF-β or IL-10, are presumably responsible for the suppression of anti-tumor immune responses and for successful tumor escape. On the other hand, in cancers associated with prominent inflammatory infiltrates, e.g., colorectal carcinoma or certain types of breast cancer, iTreg down-regulate excessive inflammation by producing ADO and/or PGE2 and protect the host from tissue injury and tumor development. Thus, iTreg utilizing the same adenosine pathway play a key but dual role in cancer, and their plasticity is controlled and driven by the microenvironment. Thus, monitoring for the frequency and functions of iTreg rather than nTreg is important in cancer. In addition, elimination of iTreg by various available strategies prior to immunotherapies may not be beneficial in all cases and needs to be undertaken with caution.

Indexed as

Gene Expression Regulation, NeoplasticAdenosineAnimalsCD4-Positive T-LymphocytesChemoradiotherapyDinoprostoneDisease ProgressionHumansImmunotherapyInflammationLymphocyte SubsetsNeoplasmsT-Lymphocytes, RegulatoryTumor EscapeTumor MicroenvironmentAdenosineDinoprostone

Identifiers

PMID24213679
PMCPMC3888225
OpenAlexW2038003693

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.