ArticleFrontiers in immunology2017
Heterogeneity of the Type I Interferon Signature in Rheumatoid Arthritis: A Potential Limitation for Its Use As a Clinical Biomarker.
Article in Frontiers in immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 2 of them syntheses that pooled it.
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Who cites it
32 citing papers in PubMed, 2 syntheses or guidelines pooled it, 57 citations in OpenAlex.
- Pooled it
- Pooled it
- Plasma interferon-alpha is associated with double-positivity for autoantibodies but is not a predictor of remission in early rheumatoid arthritis-a spin-off study of the NORD-STAR randomized clinical trial.Arthritis research & therapy · 2021Trial
- TWEAK receptor (Fn14) exacerbates TNF-α-induced inflammation in rheumatoid arthritis synovial fibroblasts and influences response to anti-TNF-α therapy.Cellular & molecular immunology · 2026Article
- Microbiota-specific serum IgG links gut and joints through immune-endothelial crosstalk in arthritis.Frontiers in microbiology · 2026Article
- Multidimensional regulatory mechanisms and translational potential of epigenetic networks in the rheumatoid arthritis disease course.Frontiers in immunology · 2026Review
- Reduced circulating anti-CXCR3 antibodies as a common hallmark bridging systemic autoimmunity and atherosclerosis.Frontiers in immunology · 2026Article
- Unveiling the prognostic and immunological role of IFI44 in glioma.Annals of medicine · 2025Article
- The Type I Interferon Axis in Systemic Autoimmune Diseases: From Molecular Pathways to Targeted Therapy.Biomolecules · 2025Review
- Complexity of the neutrophil transcriptome in early and severe rheumatoid arthritis: a role for microRNAs?Journal of leukocyte biology · 2025Article
- The Roles of T cells in Immune Checkpoint Inhibitor-Induced Arthritis.Aging and disease · 2024Review
- Role of IFN-α in Rheumatoid Arthritis.Current rheumatology reports · 2024Review
- Type I interferon pathway activation across the antiphospholipid syndrome spectrum: associations with disease subsets and systemic antiphospholipid syndrome presentation.Frontiers in immunology · 2024Article
- Clonally expanded CD38Science immunology · 2023Article
- Mechanisms underlying DMARD inefficacy in difficult-to-treat rheumatoid arthritis: a narrative review with systematic literature search.Rheumatology (Oxford, England) · 2022Review
- Interferon-α-mediated therapeutic resistance in early rheumatoid arthritis implicates epigenetic reprogramming.Annals of the rheumatic diseases · 2022Article
- Transcriptomes of peripheral blood mononuclear cells from juvenile dermatomyositis patients show elevated inflammation even when clinically inactive.Scientific reports · 2022Article
- Dynamics of Type I and Type II Interferon Signature Determines Responsiveness to Anti-TNF Therapy in Rheumatoid Arthritis.Frontiers in immunology · 2022Article
- Predictive value of drug efficacy by M6A modification patterns in rheumatoid arthritis patients.Frontiers in immunology · 2022Article
- IFI44 is an immune evasion biomarker for SARS-CoV-2 andFrontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionAn increased expression of interferon (IFN)-responding genes (IRGs), the so-called IFN signature, has been reported in rheumatoid arthritis (RA). However, some controversy exists concerning its clinical relevance. The main aim of this study is to evaluate whether quantitative and qualitative differences in the activation of the IFN pathway may account for these findings.
methodsThe expression of IFN-induced protein 44 (IFI44), IFN-induced protein 44 like (IFI44L), IFN alpha inducible protein 6, and MX dynamin-like GTPase 1 (MX1) was determined in peripheral blood in 98 RA patients (IFI6) and 28 controls. RA patients were classified into groups according to their clinical stage and treatments received: very early RA (VERA), biological disease-modifying antirheumatic drug (bDMARD) naive, and bDMARD. An additional group of 13 RA patients candidates for tumor necrosis factor alpha (TNFα) blockade was also recruited. The associations among IRGs were evaluated by network and principal component analyses.
resultsThe expression of all IRGs was increased in RA to different levels. The IFN score was increased in all RA groups (VERA, bDMARD-naïve, and bDMARD), but important differences in their degree of activation and in the relationships among IRGs were observed. The IFN score correlated with the accumulated disease activity score 28-joints, and it was found to be a predictor of clinical outcome in VERA. No differences in the IFN score were observed between the bDMARD-naive and bDMARD groups, but opposite associations with the clinical parameters were noted. Interestingly, the correlations among IRGs delineate different pictures between these two groups. The IFN score at baseline predicted poor clinical outcome upon TNFα blockade. Although no absolute changes in the IFN score were found, TNFα-blockade shifted the associations among IRGs.
conclusionA certain heterogeneity within the IFN signature can be recognized in RA, depending on the clinical stage. The structure of the IFN signature may be a potential explanation for the controversy in this field and must be considered to decipher its clinical relevancein RA.
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