Evidence map›Paper›PMID 18810759›Full record

ArticleThe Journal of pathology2008

A critical role for TRAIL in resolution of granulomatous experimental autoimmune thyroiditis.

Y Fang, G C Sharp, H Yagita, H Braley-Mullen

Open access · greenAbstract read
In one paragraph

Article in The Journal of pathology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

18 citing papers in PubMed, 37 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. IL-33 acts as a foe to MIA PaCa-2 pancreatic cancer.Medical oncology (Northwood, London, England) · 2017
    Article
  8. Trichomonas vaginalis: a possible foe to prostate cancer.Medical oncology (Northwood, London, England) · 2016
    Article
  9. Resolution of inflammation: a new therapeutic frontier.Nature reviews. Drug discovery · 2016
    Review
  10. Review
  11. Review
  12. The resolution of inflammation.Nature reviews. Immunology · 2013
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. 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

4 authors at 3 institutions in 2 countries.

Y FangResearch Service, Harry S Truman Memorial VA Hospital, University of Missouri, Columbia, MO 65212, USA. fangy@health.missouri.edu
G C Sharp
H Yagita
H Braley-Mullen
Harry S. Truman Memorial Veterans' Hospital · USJuntendo University · JPUniversity of Missouri · US

Funding

AUTOIMMUNE THYROIDITIS: MECHANISMS OF INDUCTIONR01DK035527 · NIDDK · UNIVERSITY OF MISSOURI-COLUMBIA · PI MULLEN, HELEN B · 1986 to 2007
$2.5M
NIDDK NIH HHS DK35527NIDDK NIH HHS R01 DK035527
6 · The paper itself

Abstract

Granulomatous experimental autoimmune thyroiditis (G-EAT) is induced by mouse thyroglobulin (MTG)-sensitized splenocytes activated in vitro with MTG and IL-12. Thyroid lesions reach maximal severity 20 days after cell transfer, and usually resolve or progress to fibrosis by day 60 depending on the extent of thyroid damage at day 20. Our previous studies indicated that neutralization of TNF-alpha or FasL had no effect on G-EAT induction, but neutralization of TNF-alpha promoted, while neutralization of FasL inhibited, G-EAT resolution. TNF-related apoptosis-inducing ligand (TRAIL) is a member of the TNF superfamily. This study was undertaken to define the role of endogenous TRAIL in G-EAT development and/or resolution. Neutralization of endogenous TRAIL had little effect on G-EAT induction, but significantly inhibited G-EAT resolution and increased thyroid fibrosis. This correlated with higher expression of pro-inflammatory cytokines and preferential expression of the pro-apoptotic molecule TRAIL, and anti-apoptotic molecules FLIP and Bcl-xL on inflammatory cells in thyroids of anti-TRAIL-treated recipients. The results suggest that endogenous TRAIL is not required for G-EAT development in recipients, but is critical for G-EAT resolution. Endogenous TRAIL might promote resolution, at least in part, through modulation of the balance between pro- and anti-inflammatory cytokines, and the expression pattern of pro- and anti-apoptotic molecules of thyroid epithelial cells (TECs) and inflammatory cells.

Indexed as

AnimalsAntibodies, MonoclonalApoptosisCells, CulturedInflammationInterleukin-10MiceMice, Inbred CBAMice, TransgenicMicroscopy, FluorescenceModels, AnimalReverse Transcriptase Polymerase Chain ReactionThyroiditis, AutoimmuneThyroiditis, SubacuteTNF-Related Apoptosis-Inducing LigandAntibodies, MonoclonalInterleukin-10TNF-Related Apoptosis-Inducing Ligand

Identifiers

PMID18810759
PMCPMC2637621
OpenAlexW2137928495

What OpenQuestion holds

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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.