Evidence map›Paper›PMID 23165310›Full record

ReviewCytokine & growth factor reviews2013

The emerging role of Interleukin 27 in inflammatory arthritis and bone destruction.

Iannis E Adamopoulos, Stefan Pflanz

Open access · greenAbstract readReview
In one paragraph

Review in Cytokine & growth factor reviews, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 20% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Common Polymorphisms in IL-27 Genes May Contribute to Risk of Various Human Diseases in Asian Populations: A Meta-Analysis.Medical science monitor : international medical journal of experimental and clinical research · 2016
    Pooled it
  2. Observational
  3. Review
  4. Article
  5. Article
  6. Article
  7. IL-27 attenuates IL-23 mediated inflammatory arthritis.Clinical immunology (Orlando, Fla.) · 2023
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. IL-27 Promotes Proliferation of Human Leukemic Cell Lines Through the MAPK/ERK Signaling Pathway and Suppresses Sensitivity to Chemotherapeutic Drugs.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2016
    Article
  17. Review
  18. Review
  19. Modulation of inflammation by interleukin-27.Journal of leukocyte biology · 2013
    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

2 authors at 2 institutions in 1 country.

Iannis E AdamopoulosDivision of Rheumatology, Allergy and Clinical Immunology, School of Medicine, University of California at Davis and Institute of Pediatric and Regenerative Medicine, Shriners Hospital for Children, Sacramento, CA 95817, USA. iannis@ucdmc.ucdavis.edu
Stefan Pflanz
Gilead Sciences (United States) · USShriners Hospitals for Children - Erie · US

Funding

The IL-23/IL-17 Axis in Inflammatory ArthritisR01AR062173 · NIAMS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI LEVY, DAN · 2012 to 2025
$4.9M
NIAMS NIH HHS R01 AR062173NIAMS NIH HHS R01AR62173
6 · The paper itself

Abstract

Although the causes of inflammatory arthritis elude us, aberrant cytokine expression has been linked to joint pathology. Consequently, several approaches in the clinic and/or in clinical trials are targeting cytokines, e.g. tumor necrosis factor (TNF), Interleukin 23 (IL-23) and Interleukin 17 (IL-17), with the goal of antagonizing their respective biologic activity through therapeutic neutralizing antibodies. Such, cytokine signaling-dependent molecular networks orchestrate synovial inflammation on multiple levels including differentiation of myeloid cells to osteoclasts, the central cellular players in arthritis-associated pathologic bone resorption. Hence, understanding of the cellular and molecular mechanisms elicited by synovial cytokine networks that dictate recruitment, differentiation and activation of osteoclast precursors and osteoclasts, respectively, is central to shaping novel therapeutic options for inflammatory arthritis patients. In this article we are discussing the complex signaling interactions involved in the regulation of inflammatory arthritis and it's associated bone loss with a focus on Interleukin 27 (IL-27). The present review will discuss the primary bone-degrading cell, the osteoclast, and on how IL-27, directly or indirectly, modulates osteoclast activity in autoimmune-driven inflammatory joint diseases.

Indexed as

AnimalsArthritisBone ResorptionHumansInterleukin-17OsteoclastsReceptors, InterleukinT-LymphocytesIL27RA protein, humanInterleukin-17Receptors, Interleukin

Identifiers

PMID23165310
PMCPMC3605270
OpenAlexW2074854455

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.