Evidence map›Paper›PMID 26188076›Full record

ReviewJournal of leukocyte biology2015

The TNF-family cytokine TL1A: from lymphocyte costimulator to disease co-conspirator.

Arianne C Richard, John R Ferdinand, Françoise Meylan, Erika T Hayes, Odile Gabay, Richard M Siegel

Open access · greenAbstract readReview
In one paragraph

Review in Journal of leukocyte biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

46 citing papers in PubMed, 67 citations in OpenAlex.

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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

6 authors at 2 institutions in 2 countries.

Arianne C Richard*Immunoregulation Section, Autoimmunity Branch, NIAMS, National Institutes of Health, Bethesda, Maryland, USA; Cambridge Institute for Medical Research and Department of Medicine, University of Cambridge, Cambridge, United Kingdom; Cancer Sciences Academic Unit, Faculty of Medicine, University of Southampton, Southampton, United Kingdom.
John R Ferdinand*Immunoregulation Section, Autoimmunity Branch, NIAMS, National Institutes of Health, Bethesda, Maryland, USA; Cambridge Institute for Medical Research and Department of Medicine, University of Cambridge, Cambridge, United Kingdom; Cancer Sciences Academic Unit, Faculty of Medicine, University of Southampton, Southampton, United Kingdom.
Françoise Meylan*Immunoregulation Section, Autoimmunity Branch, NIAMS, National Institutes of Health, Bethesda, Maryland, USA; Cambridge Institute for Medical Research and Department of Medicine, University of Cambridge, Cambridge, United Kingdom; Cancer Sciences Academic Unit, Faculty of Medicine, University of Southampton, Southampton, United Kingdom.
Erika T Hayes*Immunoregulation Section, Autoimmunity Branch, NIAMS, National Institutes of Health, Bethesda, Maryland, USA; Cambridge Institute for Medical Research and Department of Medicine, University of Cambridge, Cambridge, United Kingdom; Cancer Sciences Academic Unit, Faculty of Medicine, University of Southampton, Southampton, United Kingdom.
Odile Gabay*Immunoregulation Section, Autoimmunity Branch, NIAMS, National Institutes of Health, Bethesda, Maryland, USA; Cambridge Institute for Medical Research and Department of Medicine, University of Cambridge, Cambridge, United Kingdom; Cancer Sciences Academic Unit, Faculty of Medicine, University of Southampton, Southampton, United Kingdom.
Richard M Siegel*Immunoregulation Section, Autoimmunity Branch, NIAMS, National Institutes of Health, Bethesda, Maryland, USA; Cambridge Institute for Medical Research and Department of Medicine, University of Cambridge, Cambridge, United Kingdom; Cancer Sciences Academic Unit, Faculty of Medicine, University of Southampton, Southampton, United Kingdom rsiegel@nih.gov.
National Institute of Arthritis and Musculoskeletal and Skin Diseases · USNational Institutes of Health · US

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
TNFR1 in the regulation of autoinflammatory diseasesZIAAR041175 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI SIEGEL, RICHARD M · 2009 to 2019
$6.5M
Intramural NIH HHS
6 · The paper itself

Abstract

Originally described in 2002 as a T cell-costimulatory cytokine, the tumor necrosis factor family member TNF-like factor 1A (TL1A), encoded by the TNFSF15 gene, has since been found to affect multiple cell lineages through its receptor, death receptor 3 (DR3, encoded by TNFRSF25) with distinct cell-type effects. Genetic deficiency or blockade of TL1A-DR3 has defined a number of disease states that depend on this cytokine-receptor pair, whereas excess TL1A leads to allergic gastrointestinal inflammation through stimulation of group 2 innate lymphoid cells. Noncoding variants in the TL1A locus are associated with susceptibility to inflammatory bowel disease and leprosy, predicting that the level of TL1A expression may influence host defense and the development of autoimmune and inflammatory diseases.

Indexed as

AnimalsAutoimmune DiseasesDisease Models, AnimalHumansLymphocyte ActivationReceptors, Death DomainT-LymphocytesTumor Necrosis Factor Ligand Superfamily Member 15Receptors, Death DomainTumor Necrosis Factor Ligand Superfamily Member 15autoimmune diseaseDR3

Identifiers

PMID26188076
PMCPMC4763597
OpenAlexW2329080061

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.