Evidence map›Paper›PMID 31087644›Full record

ReviewImmunology2019

Intratumoral regulatory T cells: markers, subsets and their impact on anti-tumor immunity.

Hiroshi Yano, Lawrence P Andrews, Creg J Workman, Dario A A Vignali

Open access · greenAbstract readReview
In one paragraph

Review in Immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
7.3field-weighted citation impact, top 2% 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

71 citing papers in PubMed, 116 citations in OpenAlex.

  1. SRSF3 determines TScience advances · 2026
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  20. Targeting T regulatory (TCancer drug resistance (Alhambra, Calif.) · 2024
    Review

11 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

4 authors at 1 institution in 1 country.

Hiroshi YanoDepartment of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.ORCID 0000-0002-3098-2629
Lawrence P AndrewsDepartment of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
Creg J WorkmanDepartment of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
Dario A A VignaliDepartment of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.ORCID 0000-0002-2771-5992
University of Pittsburgh · US

Funding

Synergies among inhibitory receptors in tolerance, cancer & antiviral immunityP01AI108545 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI E. John Wherry · 2015 to 2026
$30.8M
Structure, Function and Mechanistic Analysis of LAG3R01AI144422 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Roy A Mariuzza, Dario AA Vignali · 2019 to 2026
$5.9M
Multimolecular Interactions During TCR RecognitionR01AI039480 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI VIGNALI, DARIO AA · 2001 to 2011
$3.6M
Interleukin-35 and the tumor microenvironmentR01CA203689 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI VIGNALI, DARIO AA · 2016 to 2020
$1.9M
NCI NIH HHS R01 CA203689NIAID NIH HHS P01 AI108545NIAID NIH HHS R01 AI039480NIAID NIH HHS R01 AI144422
6 · The paper itself

Abstract

Regulatory T (Treg) cells play a crucial role in maintaining self-tolerance and resolution of immune responses by employing multifaceted immunoregulatory mechanisms. However, Treg cells readily infiltrate into the tumor microenvironment (TME) and dampen anti-tumor immune responses, thereby becoming a barrier to effective cancer immunotherapy. There has been a substantial expansion in the development of novel immunotherapies targeting various inhibitory receptors (IRs), such as CTLA4, PD1 and LAG3, but these approaches have mechanistically focused on the elicitation of anti-tumor responses. However, enhanced inflammation in the TME could also play a detrimental role by facilitating the recruitment, stability and function of Treg cells by up-regulating chemokines that promote Treg cell migration, and/or increasing inhibitory cytokine production. Furthermore, IR blockade may enhance Treg cell function and survival, thereby serving as a resistance mechanism against effective immunotherapy. Given that Treg cells are comprised of functionally and phenotypically heterogeneous sub-populations that may alter their characteristics in a context-dependent manner, it is critical to identify unique molecular pathways that are preferentially used by intratumoral Treg cells. In this review, we discuss markers that serve to identify certain Treg cell subsets, distinguished by chemokine receptors, IRs and cytokines that facilitate their migration, stability and function in the TME. We also discuss how these Treg cell subsets correlate with the clinical outcome of patients with various types of cancer and how they may serve as potential TME-specific targets for novel cancer immunotherapies.

Indexed as

Tumor EscapeAnimalsChemokinesHumansInflammation MediatorsLymphocytes, Tumor-InfiltratingNeoplasmsPhenotypeReceptors, ChemokineSignal TransductionT-Lymphocytes, RegulatoryTumor MicroenvironmentChemokinesInflammation MediatorsReceptors, Chemokinechemokine/chemokine receptorscytokinesinhibitory/activating receptorsregulatory T cellstumor immunology

Identifiers

PMID31087644
PMCPMC6587321
OpenAlexW2945947513

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.