Evidence map›Paper›PMID 31321075›Full record

ArticleRMD open2019

IL-6-PAD4 axis in the earliest phase of arthritis in knock-in gp130F759 mice, a model for rheumatoid arthritis.

Ayano Yahagi, Taro Saika, Hiroyasu Hirano, Miwa Takai-Imamura, Fumio Tsuji, Hiroyuki Aono, Masanori Iseki, Yoshitaka Morita, Hideya Igarashi, Yukihiko Saeki and 1 more

Open access · goldAbstract readComparative Study
In one paragraph

Article in RMD open, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

13 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
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  5. Macrophages in the inflammatory response to endotoxic shock.Immunity, inflammation and disease · 2024
    Review
  6. Challenges and opportunities in animal models of psoriatic arthritis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Review
  7. Article
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  9. Review
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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.

Ayano YahagiImmunology and Molecular Genetics, Kawasaki Medical School, Kurashiki, Japan.
Taro SaikaOtorhinolaryngology, Kawasaki Medical School, Kurashiki, Japan.
Hiroyasu HiranoRheumatology, Kawasaki Medical School, Kurashiki, Japan.
Miwa Takai-ImamuraR&D Division, Ayumi Pharmaceutical Corp, Kyoto, Japan.
Fumio TsujiNara Research and Development Center, Santen Pharmaceutical Co Ltd, Nara, Japan.
Hiroyuki AonoR&D Division, Ayumi Pharmaceutical Corp, Kyoto, Japan.
Masanori IsekiImmunology and Molecular Genetics, Kawasaki Medical School, Kurashiki, Japan.
Yoshitaka MoritaRheumatology, Kawasaki Medical School, Kurashiki, Japan.
Hideya IgarashiImmunology and Molecular Genetics, Kawasaki Medical School, Kurashiki, Japan.
Yukihiko SaekiDepartment of Clinical Research, National Hospital Organization, Osaka Minami Medical Center, Kawachinagano, Japan.
Katsuhiko IshiharaImmunology and Molecular Genetics, Kawasaki Medical School, Kurashiki, Japan.ORCID 0000-0002-2826-5188
Kawasaki Medical School · JPOsaka Minami Medical Center · JPSanten (Japan) · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: Animal models for human diseases are especially valuable for clarifying molecular mechanisms before or around the onset. As a model for rheumatoid arthritis (RA), we utilise knock-in mice gp130F759. They have a Y759F mutation in gp130, a common receptor subunit for interleukin 6 (IL-6) family cytokines. Definitive arthritis develops around 8 months old and the incidence reaches 100% around 1 year old. Careful examination in the clinical course revealed very subtle resistance in flexibility of joints at 5 months old. Therefore, pathophysiological changes in gp130F759 were examined to dissect molecular mechanisms for preclinical phase of RA. Methods: Severity of arthritis in gp130F759 was evaluated with a clinical score system and histological quantification. Serum cytokines, autoantibodies and C reactive protein (CRP) were measured. Changes in the synovium were analysed by real-time PCR, flow cytometry and immunohistochemistry. Results: Around 5 months old, various types of cytokines, rheumatoid factor (RF), anti-circular citrullinated peptide IgM and CRP increased in the sera of gp130F759. Enhancement of neovascularisation, synovial hyperplasia and fibrosis was observed. Also, increases in haematopoietic cells dominated by innate immune cells and gene expression of Conclusion: The IL-6-PAD4 axis operates in the earliest phase of arthritis in gp130F759, implicating it in early RA.

Indexed as

AnimalsArthritis, RheumatoidAutoantibodiesC-Reactive ProteinCytokine Receptor gp130CytokinesFemaleHumansImmunoglobulin MIncidenceInterleukin-6MaleMiceMice, Inbred C57BLModels, AnimalMutationAutoantibodiesC-Reactive ProteinCytokine Receptor gp130CytokinesIl6st protein, mouseImmunoglobulin MInterleukin-6Padi4 protein, mousePeptides, CyclicProtein-Arginine DeiminasesRheumatoid Factoranti-CCPcytokinesearly rheumatoid arthritisinflammationsynovitis

Identifiers

PMID31321075
PMCPMC6606081
OpenAlexW2951451700

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Registered trials

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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.