Evidence map›Paper›PMID 15972960›Full record

ArticleThe American journal of pathology2005

Blocking of interleukin-17 during reactivation of experimental arthritis prevents joint inflammation and bone erosion by decreasing RANKL and interleukin-1.

Marije I Koenders, Erik Lubberts, Birgitte Oppers-Walgreen, Liduine van den Bersselaar, Monique M Helsen, Franco E Di Padova, Annemieke M H Boots, Hermann Gram, Leo A B Joosten, Wim B van den Berg

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 123 papers.

0numbers the graph read from it
0cells of the map it votes in
123citing papers in PubMed
12.2field-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

123 citing papers in PubMed, 306 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Plasma interleukin-23 and circulating IL-17AArthritis research & therapy · 2022
    Article
  16. Direct tissue-sensing reprograms TLR4Communications biology · 2021
    Article
  17. Review
  18. Article
  19. Interleukin-17 in rheumatoid arthritis: Trials and tribulations.The Journal of experimental medicine · 2020
    Review
  20. Review

63 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

10 authors at 3 institutions in 2 countries.

Marije I KoendersDepartment of Rheumatology, Experimental Rheumatology and Advanced Therapeutics, Radboud University Nijmegen Medical Center, 189, Geert Grooteplein Zuid 26-28, PO Box 9101, 6500 HB Nijmegen, The Netherlands. m.koenders@reuma.umcn.nl
Erik Lubberts
Birgitte Oppers-Walgreen
Liduine van den Bersselaar
Monique M Helsen
Franco E Di Padova
Annemieke M H Boots
Hermann Gram
Leo A B Joosten
Wim B van den Berg
Radboud University Nijmegen · NLNovartis (Switzerland) · CHRadboud University Medical Center · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rheumatoid arthritis is characterized by an intermittent course of disease with alternate periods of remission and relapse. T cells, and in particular the T-cell cytokine interleukin-17 (IL-17), are expected to be involved in arthritic flares. Here, we report that neutralizing endogenous IL-17 during reactivation of antigen-induced arthritis prevents joint inflammation and bone erosion. Synovial IL-17 mRNA expression was clearly up-regulated during primary arthritis and was further enhanced after antigen rechallenge. Neutralization of IL-17 significantly prevented joint swelling at day 1 of flare and significantly suppressed joint inflammation and cartilage proteoglycan depletion at day 4, as assessed by histology. Blocking IL-17 also clearly reduced bone erosions. Cathepsin K, a marker of osteoclast-like activity, and synovial RANKL mRNA expression were both suppressed. The degree of bone erosions strongly correlated with the severity of joint inflammation, suggesting that anti-IL-17 treatment reduced bone erosion by suppressing joint inflammation. Interestingly, blocking IL-17 suppressed synovial expression of both IL-1beta and tumor necrosis factor-alpha, whereas blocking IL-1 did not affect tumor necrosis factor-alpha levels. These data indicate that IL-17 is an important upstream mediator in joint pathology during flare-up of experimental arthritis.

Indexed as

AnimalsArthritis, ExperimentalArthritis, RheumatoidBone and BonesCarrier ProteinsCathepsin KCathepsinsInflammationInterleukin-1Interleukin-17JointsMembrane GlycoproteinsMiceRANK LigandReceptor Activator of Nuclear Factor-kappa BReverse Transcriptase Polymerase Chain ReactionCarrier ProteinsCathepsin KCathepsinsCtsk protein, mouseInterleukin-1Interleukin-17Membrane GlycoproteinsRANK LigandReceptor Activator of Nuclear Factor-kappa BRNA, MessengerTnfrsf11a protein, mouseTnfsf11 protein, mouseTumor Necrosis Factor-alpha

Identifiers

PMID15972960
PMCPMC1603454
OpenAlexW2151440511

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.