Evidence map›Paper›PMID 24813051›Full record

ArticleClinical and experimental immunology2014

Interleukin (IL)-17A, F and AF in inflammation: a study in collagen-induced arthritis and rheumatoid arthritis.

S Sarkar, S Justa, M Brucks, J Endres, D A Fox, X Zhou, F Alnaimat, B Whitaker, J C Wheeler, B H Jones and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.8field-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

33 citing papers in PubMed, 57 citations in OpenAlex.

  1. Trial
  2. Review
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  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. [The role of helper T cell in the pathogenesis of osteoarthritis].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2020
    Review
  11. Article
  12. Interleukin-17 in rheumatoid arthritis: Trials and tribulations.The Journal of experimental medicine · 2020
    Review
  13. Article
  14. Article
  15. Article
  16. Observational
  17. Review
  18. Endogenous stimulation is responsible for the high frequency of IL-17A-producing neutrophils in patients with rheumatoid arthritis.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2019
    Article
  19. Article
  20. IL-17 in the immunopathogenesis of spondyloarthritis.Nature reviews. Rheumatology · 2018
    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

11 authors at 3 institutions in 1 country.

S SarkarSection of Rheumatology, Department of Medicine, and the Arizona Arthritis Center, University of Arizona, Tucson, AZ, USA.
S Justa
M Brucks
J Endres
D A Fox
X Zhou
F Alnaimat
B Whitaker
J C Wheeler
B H Jones
S R Bommireddy
University of Arizona · USJanssen (United States) · USUniversity of Michigan–Ann Arbor · US

Funding

UNIQUE SURFACE STRUCTURES ON SYNOVIAL CELLSR01AR038477 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI FOX, DAVID ALAN · 1991 to 2011
$2.9M
Mentored Clinical Scientist Research Career Development AwardK08AR054323 · NIAMS · UNIVERSITY OF ARIZONA · PI SARKAR, SUJATA · 2009 to 2013
$566k
UNIQUE SURFACE STRUCTURES ON RHEUMATOID SYNOVIAL T CELLSR29AR038477 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI FOX, DAVID ALAN · 1986 to 1990
–
NIAMS NIH HHS AR054323NIAMS NIH HHS AR38477NIAMS NIH HHS K08 AR054323NIAMS NIH HHS R01 AR038477
6 · The paper itself

Abstract

Interleukin (IL)-17 plays a critical role in inflammation. Most studies to date have elucidated the inflammatory role of IL-17A, often referred to as IL-17. IL-17F is a member of the IL-17 family bearing 50% homology to IL-17A and can also be present as heterodimer IL-17AF. This study elucidates the distribution and contribution of IL-17A, F and AF in inflammatory arthritis. Neutralizing antibody to IL-17A alone or IL-17F alone or in combination was utilized in the mouse collagen-induced arthritis (CIA) model to elucidate the contribution of each subtype in mediating inflammation. IL-17A, F and AF were all increased during inflammatory arthritis. Neutralization of IL-17A reduced the severity of arthritis, neutralization of IL-17A+IL-17F had the same effect as neutralizing IL-17A, while neutralization of IL-17F had no effect. Moreover, significantly higher levels of IL-17A and IL-17F were detected in peripheral blood mononuclear cells (PBMC) from patients with rheumatoid arthritis (RA) in comparison to patients with osteoarthritis (OA). IL-17A and AF were detected in synovial fluid mononuclear cells (SFMC) in RA and OA, with IL-17A being significantly higher in RA patients. Enriched CD3(+) T cells from RA PBMCs produced singnificantly high levels of IL-17A and IL-17AF in comparison to OA peripheral blood CD3(+) T cells. IL-17A, F and AF were undetectable in T cells from SFMCs from RA and OA. While IL-17A, F, and AF were all induced during CIA, IL-17A played a dominant role. Furthermore, production of IL-17A, and not IL-17F or IL-17AF, was elevated in PBMCs, SFMCs and enriched peripheral blood CD3(+) T in RA.

Indexed as

AnimalsAntibodiesAntibodies, MonoclonalAntibodies, NeutralizingArthritis, ExperimentalArthritis, RheumatoidDisease Models, AnimalFemaleGranulocyte Colony-Stimulating FactorHumansImmunoglobulin GInterleukin-6Interleukin-7Leukocytes, MononuclearMaleMiceAntibodiesAntibodies, MonoclonalAntibodies, NeutralizingGranulocyte Colony-Stimulating FactorImmunoglobulin GInterleukin-6Interleukin-7arthritiscytokineinflammation

Identifiers

PMID24813051
PMCPMC4137849
OpenAlexW1516518272

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.