ArticleArthritis and rheumatism2012
Role of interferon regulatory factor 7 in serum-transfer arthritis: regulation of interferon-β production.
Article in Arthritis and rheumatism, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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.
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.
Who cites it
12 citing papers in PubMed, 30 citations in OpenAlex.
- Revealing Metabolic Reprogramming Genes as Biomarkers of Rheumatoid Arthritis: A Bioinformatics Study Based on Ensemble Learning Approach and Single Cell RNA Sequencing.Endocrine, metabolic & immune disorders drug targets · 2026Article
- Epigenetic silencing of SPHK1-IRF7 axis drives inflammaging in age-related meniscus degeneration via sphingolipid-immune dysregulation.Journal of orthopaedic surgery and research · 2025Article
- IRF7 orchestrates proinflammatory macrophage polarization and joint destruction in rheumatoid arthritis.Arthritis research & therapy · 2025Article
- BACH1 as a key driver in rheumatoid arthritis fibroblast-like synoviocytes identified through gene network analysis.Life science alliance · 2025Article
- Inflammation as a therapeutic target for osteoarthritis: A literature review of clinical trials.Clinical rheumatology · 2024Review
- Gene Network Analyses Identify Co-regulated Transcription Factors and BACH1 as a Key Driver in Rheumatoid Arthritis Fibroblast-like Synoviocytes.bioRxiv : the preprint server for biology · 2024Article
- A computational approach for the identification of key genes and biological pathways of chronic lung diseases: a systems biology approach.BMC medical genomics · 2023Article
- IRF7: role and regulation in immunity and autoimmunity.Frontiers in immunology · 2023Review
- Targeting transcription factors for therapeutic benefit in rheumatoid arthritis.Frontiers in immunology · 2023Review
- Undenatured Type II Collagen Ameliorates Inflammatory Responses and Articular Cartilage Damage in the Rat Model of Osteoarthritis.Frontiers in veterinary science · 2021Article
- Review
- Duality of fibroblast-like synoviocytes in RA: passive responders and imprinted aggressors.Nature reviews. Rheumatology · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
objectiveInnate immune responses activate synoviocytes and recruit inflammatory cells into the rheumatoid joint. Type I interferons (IFNs) play a role in autoimmunity, and IFN gene transcription is activated by IFN-regulatory factors (IRFs) in response to innate sensor recognition. The purpose of this study was to examine the effect of genetic deficiency of IRF-7 in a passive K/BxN serum-transfer model of arthritis.
methodsPassive-transfer arthritis was induced in IRF-7(-/-) mice, and additional groups were treated with IFNβ or poly(I-C). Clinical arthritis scoring, histologic assessment, micro-computed tomography, and synovial tissue quantitative polymerase chain reaction analysis were performed. Mouse serum was analyzed by enzyme-linked immunosorbent assay (ELISA).
resultsIn the passive K/BxN serum-transfer model, arthritis severity was significantly increased in IRF-7(-/-) mice compared with wild-type (WT) mice. In addition, expression of IFNβ in synovium and serum was decreased, potentially contributing to increased arthritis. IRF-7(-/-) mice injected with replacement IFNβ had a decrease in arthritis. Poly(I-C) treatment diminished arthritis in IRF-7(-/-) mice, restored synovial IFNβ gene expression, and increased serum levels of IFNβ. In vitro studies demonstrated that poly(I-C) stimulation of fibroblast-like synoviocytes (FLS) from IRF-7(-/-) mice resulted in increased induction of proinflammatory gene expression as compared with FLS from WT mice; however, IFNβ expression was not significantly different. In contrast, peritoneal macrophages from IRF-7(-/-) mice showed significantly less induction of IFNβ in response to poly(I-C) stimulation.
conclusionIRF-7 deficiency exacerbates arthritis and replacement treatment with IFNβ or poly(I-C) decreases arthritis severity. Both macrophage- and synoviocyte-specific roles of IRF-7 likely contribute to the increased arthritis. IRF-7 might play an antiinflammatory role in passive-transfer arthritis through regulation of macrophage IFNβ production.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.