Evidence map›Paper›PMID 22246057›Full record

ArticleInternational journal of molecular medicine2012

IL-33 regulates TNF-α dependent effects in synovial fibroblasts.

Elke Kunisch, Saritha Chakilam, Muktheshwar Gandesiri, Raimund W Kinne

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

30 citing papers in PubMed, 64 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Counteractive Effects of IL-33 and IL-37 on Inflammation in Osteoarthritis.International journal of environmental research and public health · 2022
    Article
  5. Article
  6. Review
  7. Article
  8. IL-33 in Rheumatic Diseases.Frontiers in medicine · 2021
    Review
  9. Frontiers in immunology · 2021
    Article
  10. Article
  11. Article
  12. Article
  13. Paradoxical role of Breg-inducing cytokines in autoimmune diseases.Journal of translational autoimmunity · 2019
    Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. A network map of IL-33 signaling pathway.Journal of cell communication and signaling · 2018
    Article
  20. Review
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 2 institutions in 1 country.

Elke KunischExperimental Rheumatology Unit, Department of Orthopedics, University Hospital Jena, Kloster-lausnitzer Str. 81, D-07607 Eisenberg, Germany. elke.kunisch@med.uni-jena.de
Saritha Chakilam
Muktheshwar Gandesiri
Raimund W Kinne
Jena University Hospital · DEFriedrich-Alexander-Universität Erlangen-Nürnberg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The recently described IL-33 acts as a pro-inflammatory cytokine, inducing the expression of multiple responses in the target cells. Although a nuclear localization of IL-33 has been described, its exact functional relevance is presently unknown. The present study was conducted to analyze the effects of IL-33 on the TNF-α induced synthesis of the pro-inflammatory mediators IL-6, IL-8, and monocyte chemotactic protein-1 (MCP-1) and the pro-destructive molecules matrix metalloproteinase-1 (MMP-1), MMP-3, and TIMP-1 of rheumatoid arthritis synovial fibroblast (RA-SFs) using RNA overexpression and silencing. TNF-α significantly induced IL-33 mRNA expression and protein synthesis in RA-SFs. TNF-α-induced IL-33 protein expression was mediated via p38 signaling. Immunohistochemistry for IL-33 clearly showed that nuclear translocation of IL-33 was induced in TNF-α stimulated RA-SFs. IL-33 overexpression enhanced TNF-α-induced pro-inflammatory and pro-destructive functions in RA-SFs. IL-33 silencing significantly downregulated TNF-α-induced pro-inflammatory functions, whereas TNF-α-induced pro-destructive functions were less influenced by IL-33 silencing. This study identifies IL-33 as a critical regulator/enhancer of TNF-α-induced functions in RA-SFs, pointing to a central role of this cytokine in the perpetuation of pro-inflammatory and pro-destructive processes in rheumatoid arthritis (RA) and other inflammatory and degenerative diseases.

Indexed as

Arthritis, RheumatoidCells, CulturedChemokine CCL2Down-RegulationFibroblastsHumansInterleukin-33Interleukin-6Interleukin-8InterleukinsMatrix Metalloproteinase 1Matrix Metalloproteinase 3p38 Mitogen-Activated Protein KinasesRNA InterferenceRNA, MessengerSignal TransductionCCL2 protein, humanChemokine CCL2CXCL8 protein, humanIL33 protein, humanIL6 protein, humanInterleukin-33Interleukin-6Interleukin-8InterleukinsMatrix Metalloproteinase 1Matrix Metalloproteinase 3MMP1 protein, humanMMP3 protein, humanp38 Mitogen-Activated Protein KinasesRNA, MessengerTIMP1 protein, humanTissue Inhibitor of Metalloproteinase-1Tumor Necrosis Factor-alpha

Identifiers

PMID22246057
PMCPMC3573710
OpenAlexW2022941305

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.