Evidence map›Paper›PMID 24681564›Full record

ArticleNature immunology2014

The adaptor TRAF5 limits the differentiation of inflammatory CD4(+) T cells by antagonizing signaling via the receptor for IL-6.

Hiroyuki Nagashima, Yuko Okuyama, Atsuko Asao, Takeshi Kawabe, Satoshi Yamaki, Hiroyasu Nakano, Michael Croft, Naoto Ishii, Takanori So

Open access · greenAbstract read
In one paragraph

Article in Nature immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

25 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. IL-6 in inflammation, autoimmunity and cancer.International immunology · 2021
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Review
  19. Oral CD103Mucosal immunology · 2017
    Article
  20. Article
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

9 authors at 3 institutions in 2 countries.

Hiroyuki NagashimaDepartment of Microbiology and Immunology, Tohoku University Graduate School of Medicine, Sendai, Japan.
Yuko OkuyamaDepartment of Microbiology and Immunology, Tohoku University Graduate School of Medicine, Sendai, Japan.
Atsuko AsaoDepartment of Microbiology and Immunology, Tohoku University Graduate School of Medicine, Sendai, Japan.
Takeshi KawabeDepartment of Microbiology and Immunology, Tohoku University Graduate School of Medicine, Sendai, Japan.
Satoshi YamakiDepartment of Microbiology and Immunology, Tohoku University Graduate School of Medicine, Sendai, Japan.
Hiroyasu Nakano1] Department of Immunology, Juntendo University Graduate School of Medicine, Tokyo, Japan. [2] Department of Biochemistry, Toho University School of Medicine, Tokyo, Japan.
Michael CroftDivision of Immune Regulation, La Jolla Institute, La Jolla, California, USA.
Naoto IshiiDepartment of Microbiology and Immunology, Tohoku University Graduate School of Medicine, Sendai, Japan.
Takanori SoDepartment of Microbiology and Immunology, Tohoku University Graduate School of Medicine, Sendai, Japan.
Tohoku University · JPJuntendo University · JPLa Jolla Institute for Immunology · US

Funding

The Molecular Basis of OX40 on CD4 T CellsR01AI049453 · NIAID · LA JOLLA INSTITUTE FOR IMMUNOLOGY · PI CROFT, MICHAEL · 2003 to 2012
$3.9M
NIAID NIH HHS AI049453NIAID NIH HHS R01 AI049453
6 · The paper itself

Abstract

The physiological functions of members of the tumor-necrosis factor (TNF) receptor (TNFR)-associated factor (TRAF) family in T cell immunity are not well understood. We found that in the presence of interleukin 6 (IL-6), naive TRAF5-deficient CD4(+) T cells showed an enhanced ability to differentiate into the TH17 subset of helper T cells. Accordingly, TH17 cell-associated experimental autoimmune encephalomyelitis (EAE) was greatly exaggerated in Traf5(-/-) mice. Although it is normally linked with TNFR signaling pathways, TRAF5 constitutively associated with a cytoplasmic region in the signal-transducing receptor gp130 that overlaps with the binding site for the transcription activator STAT3 and suppressed the recruitment and activation of STAT3 in response to IL-6. Our results identify TRAF5 as a negative regulator of the IL-6 receptor signaling pathway that limits the induction of proinflammatory CD4(+) T cells that require IL-6 for their development.

Indexed as

AnimalsCD4 AntigensCell DifferentiationCells, CulturedCytokine Receptor gp130Disease ProgressionEncephalomyelitis, Autoimmune, ExperimentalInterleukin-6MiceMice, Inbred StrainsMice, KnockoutMyelin-Oligodendrocyte GlycoproteinPeptide FragmentsSignal TransductionSTAT3 Transcription FactorTh17 CellsCD4 AntigensCytokine Receptor gp130Interleukin-6Myelin-Oligodendrocyte Glycoproteinmyelin oligodendrocyte glycoprotein (34-56)Peptide FragmentsSTAT3 Transcription FactorTNF Receptor-Associated Factor 5

Identifiers

PMID24681564
PMCPMC4108451
OpenAlexW2052047307

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.