Evidence map›Paper›PMID 12093872›Full record

ArticleThe Journal of experimental medicine2002

Critical roles for interleukin 1 and tumor necrosis factor alpha in antibody-induced arthritis.

Hong Ji, Allison Pettit, Koichiro Ohmura, Adriana Ortiz-Lopez, Veronique Duchatelle, Claude Degott, Ellen Gravallese, Diane Mathis, Christophe Benoist

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 149 papers.

0numbers the graph read from it
0cells of the map it votes in
149citing papers in PubMed
14.7field-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

149 citing papers in PubMed, 335 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Autoimmune Valvular Carditis Requires Endothelial Cell TNFR1 Expression.Arteriosclerosis, thrombosis, and vascular biology · 2023
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

89 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

9 authors at 3 institutions in 2 countries.

Hong JiSection on Immunology and Immunogenetics, Joslin Diabetes Center and Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02215, USA.
Allison Pettit
Koichiro Ohmura
Adriana Ortiz-Lopez
Veronique Duchatelle
Claude Degott
Ellen Gravallese
Diane Mathis
Christophe Benoist
Brigham and Women's Hospital · USBeth Israel Deaconess Medical Center · USHôpital Beaujon · FR

Funding

ARTHRITOGENIC IGS--WHAT ARE THEY? WHY ARE THEY MADE?R01AR046580 · NIAMS · JOSLIN DIABETES CENTER · PI MATHIS, DIANE J · 2000 to 2009
$3.8M
NIAMS NIH HHS 1R01 AR/AI46580-01
6 · The paper itself

Abstract

In spontaneous inflammatory arthritis of K/BxN T cell receptor transgenic mice, the effector phase of the disease is provoked by binding of immunoglobulins (Igs) to joint surfaces. Inflammatory cytokines are known to be involved in human inflammatory arthritis, in particular rheumatoid arthritis, although, overall, the pathogenetic mechanisms of the human affliction remain unclear. To explore the analogy between the K/BxN model and human patients, we assessed the role and relative importance of inflammatory cytokines in K/BxN joint inflammation by transferring arthritogenic serum into a panel of genetically deficient recipients. Interleukin (IL)-1 proved absolutely necessary. Tumor necrosis factor (TNF)-alpha was also required, although seemingly less critically than IL-1, because a proportion of TNF-alpha-deficient mice developed robust disease. There was no evidence for an important role for IL-6. Bone destruction and reconstruction were also examined. We found that all mice with strong inflammation exhibited the bone erosion and reconstruction phenomena typical of K/BxN arthritis, with no evidence of any particular requirement for TNFalpha for bone destruction. The variability in the requirement for TNF-alpha, reminiscent of that observed in treated rheumatoid arthritis patients, did not appear genetically programmed but related instead to subtle environmental changes.

Indexed as

AntibodiesAnimalsAntigens, CDArthritis, ExperimentalCytokinesDisease Models, AnimalGenetic Predisposition to DiseaseImmunization, PassiveInflammationInterleukin-1Interleukin-6MiceMice, TransgenicReceptors, Interleukin-1Receptors, Tumor Necrosis FactorReceptors, Tumor Necrosis Factor, Type IAntibodiesAntigens, CDCytokinesInterleukin-1Interleukin-6Receptors, Interleukin-1Receptors, Tumor Necrosis FactorReceptors, Tumor Necrosis Factor, Type IReceptors, Tumor Necrosis Factor, Type IITumor Necrosis Factor-alpha

Identifiers

PMID12093872
PMCPMC2194010
OpenAlexW2111935270

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.