ArticleArthritis research & therapy2016
The type I interferon signature in leukocyte subsets from peripheral blood of patients with early arthritis: a major contribution by granulocytes.
Article in Arthritis research & therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 2 of them syntheses that pooled it.
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Who cites it
24 citing papers in PubMed, 2 syntheses or guidelines pooled it, 29 citations in OpenAlex.
- Pooled it
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- Article
- Interferon-Mediated Regulation of Memory B Cell Identity and Function.Immunological reviews · 2026Review
- Antinuclear Antibodies Predict Treatment Escalation and Biologic Switching in Rheumatoid Arthritis.Diagnostics (Basel, Switzerland) · 2026Article
- The Type I Interferon Axis in Systemic Autoimmune Diseases: From Molecular Pathways to Targeted Therapy.Biomolecules · 2025Review
- Role of IFN-α in Rheumatoid Arthritis.Current rheumatology reports · 2024Review
- The Lnc-ENST00000602558/IGF1 axis as a predictor of response to treatment with tripterygium glycosides in rheumatoid arthritis patients.Immunity, inflammation and disease · 2024Article
- Gene expression signatures of target tissues in type 1 diabetes, lupus erythematosus, multiple sclerosis, and rheumatoid arthritis.Science advances · 2021Article
- Differential CpG DNA methylation in peripheral naïve CD4Clinical epigenetics · 2020Article
- Shared and unique immune alterations in pre-clinical autoimmunity.Current opinion in immunology · 2019Review
- Rheumatoid arthritis-relevant DNA methylation changes identified in ACPA-positive asymptomatic individuals using methylome capture sequencing.Clinical epigenetics · 2019Article
- Dynamics of the Type I Interferon Response During Immunosuppressive Therapy in Rheumatoid Arthritis.Frontiers in immunology · 2019Article
- The Role of Epigenetics in Autoimmune/Inflammatory Disease.Frontiers in immunology · 2019Review
- A novel gene-expression-signature-based model for prediction of response to Tripterysium glycosides tablet for rheumatoid arthritis patients.Journal of translational medicine · 2018Article
- A novel two-score system for interferon status segregates autoimmune diseases and correlates with clinical features.Scientific reports · 2018Article
- What are the dominant cytokines in early rheumatoid arthritis?Current opinion in rheumatology · 2018Review
- Chromosome conformation signatures define predictive markers of inadequate response to methotrexate in early rheumatoid arthritis.Journal of translational medicine · 2018Article
- A Novel Circulating miRNA-Based Model Predicts the Response to Tripterysium Glycosides Tablets: Moving Toward Model-Based Precision Medicine in Rheumatoid Arthritis.Frontiers in pharmacology · 2018Article
- IRF4 and IRGs Delineate Clinically Relevant Gene Expression Signatures in Systemic Lupus Erythematosus and Rheumatoid Arthritis.Frontiers in immunology · 2018Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe type I interferon (IFN) signature in rheumatoid arthritis (RA) has shown clinical relevance in relation to disease onset and therapeutic response. Identification of the cell type(s) contributing to this IFN signature could provide insight into the signature's functional consequences. The aim of this study was to investigate the contribution of peripheral leukocyte subsets to the IFN signature in early arthritis.
methodsBlood was collected from 26 patients with early arthritis and lysed directly or separated into peripheral blood mononuclear cells (PBMCs) and polymorphonuclear granulocytes (PMNs). PBMCs were sorted into CD4(+) T cells, CD8(+) T cells, CD19(+) B cells, and CD14(+) monocytes by flow cytometry. Messenger RNA expression of three interferon response genes (IRGs RSAD2, IFI44L, and MX1) and type I interferon receptors (IFNAR1 and IFNAR2) was determined in whole blood and blood cell subsets by quantitative polymerase chain reaction. IRG expression was averaged to calculate an IFN score for each sample.
resultsPatients were designated "IFN(high)" (n = 8) or "IFN(low)" (n = 18) on the basis of an IFN score cutoff in whole peripheral blood from healthy control subjects. The difference in IFN score between IFN(high) and IFN(low) patients was remarkably large for the PMN fraction (mean 25-fold) compared with the other subsets (mean 6- to 9-fold), indicating that PMNs are the main inducers of IRGs. Moreover, the relative contribution of the PMN fraction to the whole-blood IFN score was threefold higher than expected from its abundance in blood (p = 0.008), whereas it was three- to sixfold lower for the other subsets (p ≤ 0.063), implying that the PMNs are most sensitive to IFN signaling. Concordantly, IFNAR1 and IFNAR2 were upregulated compared with healthy controls selectively in patient PMNs (p ≤ 0.0077) but not in PBMCs.
conclusionsPMNs are the main contributors to the whole-blood type I IFN signature in patients with early arthritis, which seems due to increased sensitivity of these cells to type I IFN signaling. Considering the well-established role of neutrophils in the pathology of arthritis, this suggests a role of type I IFN activity in the disease as well.
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