Evidence map›Paper›PMID 18571443›Full record

ArticleImmunity2008

The TNF-family receptor DR3 is essential for diverse T cell-mediated inflammatory diseases.

Françoise Meylan, Todd S Davidson, Erin Kahle, Michelle Kinder, Krishika Acharya, Dragana Jankovic, Virgilio Bundoc, Marcus Hodges, Ethan M Shevach, Andrea Keane-Myers and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Immunity, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
112citing papers in PubMed, 1 pooled it
7.0field-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

112 citing papers in PubMed, 1 synthesis or guideline pooled it, 216 citations in OpenAlex.

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  19. The role of the DFF40/CAD endonuclease in genomic stability.Apoptosis : an international journal on programmed cell death · 2021
    Review
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52 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

12 authors at 2 institutions in 2 countries.

Françoise MeylanImmunoregulation Unit, Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892.
Todd S Davidson
Erin Kahle
Michelle Kinder
Krishika Acharya
Dragana Jankovic
Virgilio Bundoc
Marcus Hodges
Ethan M Shevach
Andrea Keane-Myers
Eddie C Y Wang
Richard M Siegel
National Institutes of Health · USCardiff University · GB

Funding

TL1A and its receptor DR3 in normal and autoimmune T cell responsesZIAAR041174 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI SIEGEL, RICHARD M · 2009 to 2019
$9.8M
Studies of the Function of Naturally Occurring and Adaptive T Regulatory CellsZ01AI000959 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI SHEVACH, ETHAN M. · 2006 to 2008
$5.1M
TL1A and its receptor DR3 in normal and autoimmune T cell responsesZ01AR041174 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI SIEGEL, RICHARD M · 2008 to 2008
$707k
Intramural NIH HHS Z01 AR041174Medical Research Council G0300180Medical Research Council G0300180(65735)Medical Research Council G0500617Medical Research Council G0500617(74644)
6 · The paper itself

Abstract

DR3 (TRAMP, LARD, WSL-1, TNFRSF25) is a death-domain-containing tumor necrosis factor (TNF)-family receptor primarily expressed on T cells. TL1A, the TNF-family ligand for DR3, can costimulate T cells, but the physiological function of TL1A-DR3 interactions in immune responses is not known. Using DR3-deficient mice, we identified DR3 as the receptor responsible for TL1A-induced T cell costimulation and dendritic cells as the likely source for TL1A during T cell activation. Despite its role in costimulation, DR3 was not required for in vivo T cell priming, for polarization into T helper 1 (Th1), Th2, or Th17 effector cell subtypes, or for effective control of infection with Toxoplasma gondii. Instead, DR3 expression was required on T cells for immunopathology, local T cell accumulation, and cytokine production in Experimental Autoimmune Encephalomyelitis (EAE) and allergic lung inflammation, disease models that depend on distinct effector T cell subsets. DR3 could be an attractive therapeutic target for T cell-mediated autoimmune and allergic diseases.

Indexed as

AnimalsCD4-Positive T-LymphocytesCell DifferentiationCell ProliferationEncephalomyelitis, Autoimmune, ExperimentalInflammationLymphocyte ActivationMiceMice, Inbred C57BLMice, TransgenicReceptors, Tumor Necrosis Factor, Member 25Respiratory HypersensitivityReverse Transcriptase Polymerase Chain ReactionT-Lymphocyte SubsetsToxoplasmosisTumor Necrosis Factor Ligand Superfamily Member 15Receptors, Tumor Necrosis Factor, Member 25Tnfrsf25 protein, mouseTnfsf15 protein, mouseTumor Necrosis Factor Ligand Superfamily Member 15

Identifiers

PMID18571443
PMCPMC2760084
OpenAlexW1978824927

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.