Evidence map›Paper›PMID 24453414›Full record

ReviewMediators of inflammation2013

The role of TL1A and DR3 in autoimmune and inflammatory diseases.

Yoshihiro Aiba, Minoru Nakamura

Open access · goldAbstract readReview
In one paragraph

Review in Mediators of inflammation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 10% 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

41 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
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  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Artemvulactone E isolated fromFrontiers in pharmacology · 2024
    Article
  11. TL1A induces apoptosis via DR3 in grass carp (Fish and shellfish immunology reports · 2023
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  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.

Yoshihiro AibaClinical Research Center, National Hospital Organization Nagasaki Medical Center, Kubara 2-1001-1, Omura 856-8562, Japan.
Minoru NakamuraClinical Research Center, National Hospital Organization Nagasaki Medical Center, Kubara 2-1001-1, Omura 856-8562, Japan ; Department of Hepatology, Nagasaki University Graduate School of Biomedical Sciences, Kubara 2-1001-1, Omura 856-8562, Japan ; Headquarters of PBC Research in NHOSLJ, Clinical Research Center, National Hospital Organization Nagasaki Medical Center, Kubara 2-1001-1, Omura 856-8562, Japan.
Nagasaki Medical Center · JPNagasaki University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

TNF-like ligand 1A (TL1A), which binds its cognate receptor DR3 and the decoy receptor DcR3, is an identified member of the TNF superfamily. TL1A exerts pleiotropic effects on cell proliferation, activation, and differentiation of immune cells, including helper T cells and regulatory T cells. TL1A and its two receptors expression is increased in both serum and inflamed tissues in autoimmune diseases such as inflammatory bowel disease (IBD), rheumatoid arthritis (RA), and ankylosing spondylitis (AS). Polymorphisms of the TNFSF15 gene that encodes TL1A are associated with the pathogenesis of irritable bowel syndrome, leprosy, and autoimmune diseases, including IBD, AS, and primary biliary cirrhosis (PBC). In mice, blocking of TL1A-DR3 interaction by either antagonistic antibodies or deletion of the DR3 gene attenuates the severity of multiple autoimmune diseases, whereas sustained TL1A expression on T cells or dendritic cells induces IL-13-dependent small intestinal inflammation. This suggests that modulation of TL1A-DR3 interaction may be a potential therapeutic target in several autoimmune diseases, including IBD, RA, AS, and PBC.

Indexed as

AnimalsArthritis, RheumatoidAutoimmune DiseasesHumansInflammationInflammatory Bowel DiseasesPsoriasisReceptors, Tumor Necrosis Factor, Member 25Signal TransductionTh17 CellsTh1 CellsTh2 CellsT-Lymphocytes, RegulatoryTumor Necrosis Factor Ligand Superfamily Member 15Receptors, Tumor Necrosis Factor, Member 25Tumor Necrosis Factor Ligand Superfamily Member 15

Identifiers

PMID24453414
PMCPMC3880748
OpenAlexW2006563647

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.