Evidence map›Paper›PMID 20826539›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2011

Naive and activated T cells display differential responsiveness to TL1A that affects Th17 generation, maintenance, and proliferation.

Gareth W Jones, Jason S Stumhofer, Tom Foster, Jason P Twohig, Paul Hertzog, Nicholas Topley, Anwen S Williams, Christopher A Hunter, Brendan J Jenkins, Eddie C Y Wang and 1 more

Open access · greenAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

33 citing papers in PubMed, 51 citations in OpenAlex.

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  11. Activation of naïve CD4Nature immunology · 2019
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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

11 authors at 4 institutions in 4 countries.

Gareth W JonesDepartment of Infection, Immunity and Biochemistry, School of Medicine, Cardiff University, Heath Park, Cardiff, CF14 4XN, Wales, UK.
Jason S Stumhofer
Tom Foster
Jason P Twohig
Paul Hertzog
Nicholas Topley
Anwen S Williams
Christopher A Hunter
Brendan J Jenkins
Eddie C Y Wang
Simon A Jones
Institute of Infection and Immunity · CACardiff University · GBUniversity of Pennsylvania · USMonash Institute of Medical Research · AU

Funding

Regulation of the early immune response to toxoplasma gondiiR01AI042334 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI HUNTER, CHRISTOPHER A · 1998 to 2013
$4.1M
Arthritis Research UK 18286Arthritis Research UK ARC19234Medical Research Council G0300180Medical Research Council G0300180(65735)Medical Research Council G0901119Medical Research Council G0901119(91900)NIAID NIH HHS AI42334NIAID NIH HHS R01 AI042334Versus Arthritis 18286Wellcome Trust
6 · The paper itself

Abstract

Tumor necrosis factor (TNF)-like cytokine (TL1A) is a T-cell costimulator that bolsters cytokine-induced activation through death receptor 3 (DR3). To explore the relationship between T-cell activation and TL1A responsiveness, flow cytometry profiled DR3 expression in resting and activated T cells. In human CD4(+) T cells, DR3 was induced rapidly following activation and expressed prominently by interleukin (IL)-17-secreting T cells (Th17). Splenic T cells from wild-type and DR3-deficient mice showed that TL1A activation of DR3 inhibits Th17 generation (81 ± 2.6% at 100 ng/ml TL1A) from naive T cells. This response was not associated with suppression of T-cell proliferation. Using neutralizing antibodies or T cells derived from genetically modified mice, TL1A inhibition of Th17 development was found to be independent of IL-2, IL-27, γIFN, IFNAR1, and STAT1. Under suboptimal TCR activation, TL1A continued to block IL-17A secretion, however, the reduced threshold of TCR engagement was now linked with an increase in TL1A-driven proliferation. In contrast, fully committed Th17 cells displayed an altered TL1A responsiveness and in the absence of TCR costimulation supported the maintenance of T cell IL-17A expression. Consequently, TL1A orchestrates unique outcomes in naive and effector T-helper cells, which may affect the proliferation, differentiation and maintenance of Th17 cells in peripheral compartments and inflamed tissues.

Indexed as

AnimalsCD4-Positive T-LymphocytesCell DifferentiationCell ProliferationCells, CulturedDose-Response Relationship, DrugFemaleFlow CytometryHumansInterleukin-17Interleukin-2Interleukin-21InterleukinsLymphocyte ActivationMaleMiceInterleukin-17Interleukin-2Interleukin-21InterleukinsReceptors, Tumor Necrosis Factor, Member 25Transforming Growth Factor betaTumor Necrosis Factor Ligand Superfamily Member 15

Identifiers

PMID20826539
PMCPMC3005434
OpenAlexW2047504529

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.