Evidence map›Paper›PMID 20173391›Full record

ReviewCurrent directions in autoimmunity2010

TNF-alpha: an activator of CD4+FoxP3+TNFR2+ regulatory T cells.

Xin Chen, Joost J Oppenheim

Registry-linked trialAbstract readReview
In one paragraph

Review in Current directions in autoimmunity, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02765126 (Clifford Craig Vaccine Trial Centre), which is not on this map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
18.0field-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.

NCT02765126 naunknown statusnot on this mapstarted 2016, after this paper: background citation

Clifford Craig Vaccine Trial Centre: Heterologous Effect of Diptheria, Tetanus, Acellular Pertussis Vaccination on Influenza Vaccine Challenge in the Elderly

TypeinterventionalSponsorClifford Craig Medical Research TrustRan2016 to 2019Enrolled450ConditionsHeterologous Effects of VaccinesArmsSeasonal influenza vaccine, Diphtheria-tetanus-acellular pertussis vaccine
3 · Its place in the literature

Who cites it

55 citing papers in PubMed, 110 citations in OpenAlex.

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  16. TNF-TNFR2 Signal Plays a Decisive Role in the Activation of CD4Advances in experimental medicine and biology · 2021
    Article
  17. Article
  18. Review
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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

2 authors at 2 institutions in 1 country.

Xin ChenBasic Science Program, SAIC-Frederick, Inc., National Cancer Institute-Frederick, MD 21702, USA. chenxin@mail.nih.gov
Joost J Oppenheim
Center for Cancer Research · USScience Applications International Corporation (United States) · US

Funding

Role of T regulatory suppression in autoimmunity and cancerZIABC010707 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI OPPENHEIM, JOOST J · 2009 to 2022
$4.9M
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 BC010707NCI NIH HHS N01 CO012400NCI NIH HHS N01-CO-12400
6 · The paper itself

Abstract

TNF-alpha (TNF) is a pleiotropic cytokine which can have proinflammatory or immunosuppressive effects, depending on the context, duration of exposure and disease state. The basis for the opposing actions of TNF remains elusive. The growing appreciation of CD4+FoxP3+ regulatory T cells (Tregs), which comprise approximately 10% of peripheral CD4 cells, as pivotal regulators of immune responses has provided a new framework to define the cellular and molecular basis underlying the contrasting action of TNF. TNF by itself can overcome the profound anergic state of T cell receptor-stimulated Tregs. Furthermore, in concert with IL-2, TNF selectively activates Tregs, resulting in proliferation, upregulation of FoxP3 expression and increases in their suppressive activity. Both human and mouse Tregs predominantly express TNFR2, making it possible for TNF to enhance Treg activity, which helps limit the collateral damage caused by excessive immune responses and eventually terminates immune response. TNFR2-expressing CD4+FoxP3+ Tregs comprise approximately 40% of peripheral Tregs in normal mice and present the maximally suppressive subset of Tregs. In this review, studies describing the action of TNF on Treg function will be discussed. The role of Tregs in the autoimmune disorders and cancer as well as the effect of anti-TNF therapy on Tregs, especially in rheumatoid arthritis, will also be considered.

Indexed as

AnimalsAutoimmune DiseasesForkhead Transcription FactorsHumansInflammationInterleukin-2Lymphocyte ActivationMiceModels, ImmunologicalPertussis ToxinReceptors, Tumor Necrosis Factor, Type IIT-Lymphocytes, RegulatoryTumor Necrosis Factor-alphaForkhead Transcription FactorsFOXP3 protein, humanFoxp3 protein, mouseInterleukin-2Pertussis ToxinReceptors, Tumor Necrosis Factor, Type IITumor Necrosis Factor-alpha

Identifiers

PMID20173391
PMCPMC6314650
OpenAlexW1508779235

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.