Evidence map›Paper›PMID 38881847›Full record

ArticleExperimental biology and medicine (Maywood, N.J.)2024

TLR3 signaling-induced interferon-stimulated gene 56 plays a role in the pathogenesis of rheumatoid arthritis.

Hikaru Kristi Ishibashi, Yuzuru Nakamura, Tatsuro Saruga, Tadaatsu Imaizumi, Akira Kurose, Shogo Kawaguchi, Kazuhiko Seya, Eiji Sasaki, Yasuyuki Ishibashi

Abstract read
In one paragraph

Article in Experimental biology and medicine (Maywood, N.J.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

2 citing papers in PubMed.

  1. Article
  2. 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

9 authors.

Hikaru Kristi IshibashiDepartment of Orthopaedic Surgery, Hirosaki University Graduate School of Medicine, Hirosaki, Aomori, Japan.
Yuzuru NakamuraDepartment of Orthopaedic Surgery, Hirosaki University Graduate School of Medicine, Hirosaki, Aomori, Japan.
Tatsuro SarugaDepartment of Orthopaedic Surgery, Hirosaki University Graduate School of Medicine, Hirosaki, Aomori, Japan.
Tadaatsu ImaizumiDepartment of Vascular Biology, Hirosaki University Graduate School of Medicine, Hirosaki, Aomori, Japan.
Akira KuroseDepartment of Anatomic Pathology, Hirosaki University Graduate School of Medicine, Hirosaki, Aomori, Japan.
Shogo KawaguchiDepartment of Vascular Biology, Hirosaki University Graduate School of Medicine, Hirosaki, Aomori, Japan.
Kazuhiko SeyaDepartment of Vascular Biology, Hirosaki University Graduate School of Medicine, Hirosaki, Aomori, Japan.
Eiji SasakiDepartment of Orthopaedic Surgery, Hirosaki University Graduate School of Medicine, Hirosaki, Aomori, Japan.
Yasuyuki IshibashiDepartment of Orthopaedic Surgery, Hirosaki University Graduate School of Medicine, Hirosaki, Aomori, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rheumatoid fibroblast-like synoviocytes (RFLS) have an important role in the inflammatory pathogenesis of rheumatoid arthritis (RA). Toll-like receptor 3 (TLR3) is upregulated in RFLS; its activation leads to the production of interferon-β (IFN-β), a type I IFN. IFN-stimulated gene 56 (ISG56) is induced by IFN and is involved in innate immune responses; however, its role in RA remains unknown. Therefore, the purpose of this study was to investigate the role of TLR3-induced ISG56 in human RFLS. RFLS were treated with polyinosinic-polycytidylic acid (poly I:C), which served as a TLR3 ligand. ISG56, melanoma differentiation-associated gene 5 (MDA5), and C-X-C motif chemokine ligand 10 (CXCL10) expression were measured using quantitative reverse transcription-polymerase chain reaction, western blotting, and enzyme-linked immunosorbent assay. Using immunohistochemistry, we found that ISG56 was expressed in synovial tissues of patients with RA and osteoarthritis. Under poly I:C treatment, ISG56 was upregulated in RFLS. In addition, we found that the type I IFN-neutralizing antibody mixture suppressed ISG56 expression. ISG56 knockdown decreased CXCL10 expression and MDA5 knockdown decreased ISG56 expression. In addition, we found that ISG56 was strongly expressed in the synovial cells of patients with RA. TLR3 signaling induced ISG56 expression in RFLS and type I IFN was involved in ISG56 expression. ISG56 was also found to be associated with CXCL10 expression, suggesting that ISG56 may be involved in TLR3/type I IFN/CXCL10 axis, and play a role in RA synovial inflammation.

Indexed as

Adaptor Proteins, Signal TransducingArthritis, RheumatoidSignal TransductionToll-Like Receptor 3Cells, CulturedChemokine CXCL10HumansInterferon-Induced Helicase, IFIH1Poly I-CRNA-Binding ProteinsSynoviocytesAdaptor Proteins, Signal TransducingChemokine CXCL10CXCL10 protein, humanIFIH1 protein, humanIFIT1 protein, humanInterferon-Induced Helicase, IFIH1Poly I-CRNA-Binding ProteinsTLR3 protein, humanToll-Like Receptor 3CXCL10ISG56rheumatoid arthritissynovitisTLR3

Identifiers

PMID38881847
PMCPMC11176439

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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.