Evidence map›Paper›PMID 18525350›Full record

ReviewCurrent opinion in rheumatology2008

The interleukin-23/interleukin-17 axis in spondyloarthritis.

Gerlinde Layh-Schmitt, Robert A Colbert

Abstract readReview
In one paragraph

Review in Current opinion in rheumatology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

28 citing papers in PubMed, 65 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Journal of immunology research · 2022
    Article
  6. Recent Updates in Juvenile Spondyloarthritis.Rheumatic diseases clinics of North America · 2021
    Review
  7. Review
  8. Review
  9. Article
  10. The synovio-entheseal complex in enthesoarthritis.Clinical and experimental medicine · 2016
    Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Update on juvenile spondyloarthritis.Rheumatic diseases clinics of North America · 2013
    Review
  17. Review
  18. Article
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

Gerlinde Layh-SchmittWilliam S. Rowe Division of Rheumatology, Department of Pediatrics, Cincinnati Children's Hospital Medical Center and Cincinnati Children's Research Foundation, Cincinnati, Ohio, USA.
Robert A Colbert
Cincinnati Children's Hospital Medical Center · US

Funding

Pathogenic Mechanisms in SpondyloarthritisZIAAR041184 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI COLBERT, ROBERT · 2009 to 2025
$47.6M
Intramural NIH HHS ZIA AR041184
6 · The paper itself

Abstract

purpose of reviewTo inform readers of recent advances in our understanding of the development and function of Th17 T cells and emerging data suggesting that the interleukin-23/interleukin-17 axis may be involved in the pathogenesis of spondyloarthritis. RECENT

findingsThe discovery of CD4+ Th17 T cells and the interleukin-23/interleukin-17 axis has challenged existing paradigms and the role of Th1 T cells in many autoimmune diseases. The development and cytokine profile of Th17 T cells differs in mice and humans. In humans, interleukin-23 synergizes with interleukin-6 and interleukin-1 to promote Th17 development. In mice, transforming growth factor-beta and interleukin-6 are critical, whereas interleukin-23 is more important at later stages promoting interleukin-17 production. In mice, CD4+ cells producing interferon-gamma appear to be distinct from interleukin-17-producing cells, while in humans cells secreting both cytokines have been observed. Growing evidence from animal models, cytokine analyses of patient fluids, and whole-genome association studies suggest that the interleukin-23/interleukin-17 axis plays an important role in spondyloarthritis pathogenesis. Possible links between an HLA-B27-induced unfolded protein response and activation of the interleukin-23/interleukin-17 axis have been observed in animal models and may contribute to the development of the spondyloarthritis phenotype. SUMMARY: Activation of the interleukin-23/interleukin-17 axis in spondyloarthritis has important therapeutic implications.

Indexed as

CD4-Positive T-LymphocytesCytokinesHLA-B27 AntigenHumansInterleukin-17Interleukin-23Polymorphism, GeneticReceptors, InterleukinSpondylarthropathiesCytokinesHLA-B27 AntigenIL23R protein, humanInterleukin-17Interleukin-23Receptors, Interleukin

Identifiers

PMID18525350
PMCPMC3494971
OpenAlexW1992892304

What OpenQuestion holds

Textmetadata
LicenceTDM
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.