Evidence map›Paper›PMID 17609389›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2007

TNF-induced structural joint damage is mediated by IL-1.

Jochen Zwerina, Kurt Redlich, Karin Polzer, Leo Joosten, Gerhard Krönke, Joerg Distler, Andreas Hess, Noreen Pundt, Thomas Pap, Oskar Hoffmann and 5 more

Open access · greenAbstract readComparative Study
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers.

0numbers the graph read from it
0cells of the map it votes in
111citing papers in PubMed
18.8field-weighted citation impact, top 1% 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

111 citing papers in PubMed, 296 citations in OpenAlex.

  1. Article
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  11. The role of exercise in aromatase inhibitor-induced arthralgia.PM & R : the journal of injury, function, and rehabilitation · 2024
    Review
  12. eLife · 2024
    Article
  13. Article
  14. Review
  15. Role of Interleukin-36 in inflammatory joint diseases.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2023
    Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article

51 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

15 authors at 7 institutions in 5 countries.

Jochen ZwerinaDepartment of Internal Medicine III, Medical University of Vienna, A-1090 Vienna, Austria.
Kurt Redlich
Karin Polzer
Leo Joosten
Gerhard Krönke
Joerg Distler
Andreas Hess
Noreen Pundt
Thomas Pap
Oskar Hoffmann
Juerg Gasser
Clemens Scheinecker
Josef S Smolen
Wim van den Berg
Georg Schett
Friedrich-Alexander-Universität Erlangen-Nürnberg · DEMedical University of Vienna · ATRadboud University Medical Center · NLUniversity Hospital Münster · DENovartis Institutes for BioMedical ResearchUniversity of Colorado Health · USUniversity of Vienna · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Blocking TNF effectively inhibits inflammation and structural damage in human rheumatoid arthritis (RA). However, so far it is unclear whether the effect of TNF is a direct one or indirect on up-regulation of other mediators. IL-1 may be one of these candidates because it has a central role in animal models of arthritis, and inhibition of IL-1 is used as a therapy of human RA. We removed the effects of IL-1 from a TNF-mediated inflammatory joint disease by crossing IL-1alpha and beta-deficient mice (IL-1-/-) with arthritic human TNF-transgenic (hTNFtg) mice. Development of synovial inflammation was almost unaffected on IL-1 deficiency, but bone erosion and osteoclast formation were significantly reduced in IL-1-/-hTNFtg mice, compared with hTNFtg mice based on an intrinsic differentiation defect of IL-1-deficient monocytes. Most dramatically, however, cartilage damage was absent in IL-1-/-hTNFtg mice. Chimera studies revealed that protection of cartilage is based on the loss of IL-1 on hematopoietic, but not mesenchymal, cells, leading to decreased expression of ADAMTS-5 and MMP-3. These data show that TNF-mediated cartilage damage is completely and TNF-mediated bone damage is partially dependent on IL-1, suggesting that IL-1 is a crucial mediator for inflammatory cartilage and bone degradation.

Indexed as

AnimalsArthritis, RheumatoidCells, CulturedHumansInterleukin-1MiceMice, KnockoutMice, TransgenicTumor Necrosis Factor-alphaWeight LossInterleukin-1Tumor Necrosis Factor-alpha

Identifiers

PMID17609389
PMCPMC1913858
OpenAlexW2045553984

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.