Evidence map›Paper›PMID 22017439›Full record

ReviewImmunological reviews2011

TL1A and DR3, a TNF family ligand-receptor pair that promotes lymphocyte costimulation, mucosal hyperplasia, and autoimmune inflammation.

Françoise Meylan, Arianne C Richard, Richard M Siegel

Abstract readReview
In one paragraph

Review in Immunological reviews, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

77 citing papers in PubMed, 129 citations in OpenAlex.

  1. Article
  2. Article
  3. A high throughput assay to identify modulators of Death Receptor 3 (DR3).SLAS discovery : advancing life sciences R & D · 2026
    Article
  4. TL1A Inhibition in Inflammatory Bowel Disease: A Pipeline Review.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2025
    Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. TL1A induces apoptosis via DR3 in grass carp (Fish and shellfish immunology reports · 2023
    Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

17 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

3 authors at 2 institutions in 1 country.

Françoise MeylanImmunoregulation Section, Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Arianne C Richard
Richard M Siegel
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
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 AR041174
6 · The paper itself

Abstract

DR3 (TNFRSF25) is a member of the tumor necrosis factor receptor (TNFR) superfamily expressed primarily on lymphocytes and is a receptor for the TNF family cytokine TL1A (TNFSF15). DR3 costimulates T-cell activation, but it is unique among these receptors in that it signals through an intracytoplasmic death domain and the adapter protein TRADD (TNFR-associated death domain). TL1A costimulates T cells to produce a wide variety of cytokines and can promote expansion of activated and regulatory T cells in vivo. Studies in mice deficient in DR3 or TL1A or in animals treated with antibodies that block the activity of TL1A have revealed a specific role for DR3 in enhancing effector T-cell proliferation at the site of tissue inflammation in autoimmune disease models. DR3 appears to be required in autoimmune disease models dependent on a variety of different T-cell subsets and also invariant natural killer T (iNKT) cells. Chronic expression of TL1A induces a distinct interleukin-13-dependent pathology in the small intestine marked by goblet cell hyperplasia and other features associated with allergic and anti-parasitic responses. These studies suggest that TL1A may be a viable target for therapies designed to inhibit the T-cell-dependent component of diverse autoimmune diseases.

Indexed as

Immunity, InnateAnimalsAsthmaAutoimmunityCell ProliferationCytokinesGene ExpressionHumansInflammatory Bowel DiseasesKiller Cells, NaturalLymphocyte ActivationMiceMice, KnockoutReceptors, Tumor Necrosis Factor, Member 25Signal TransductionT-LymphocytesCytokinesReceptors, Tumor Necrosis Factor, Member 25TNF Receptor-Associated Death Domain ProteinTnfrsf25 protein, mouseTnfsf15 protein, mouseTumor Necrosis Factor Ligand Superfamily Member 15

Identifiers

PMID22017439
PMCPMC3882070
OpenAlexW2162490282

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.