ArticleJournal of leukocyte biology2025
Complexity of the neutrophil transcriptome in early and severe rheumatoid arthritis: a role for microRNAs?
Article in Journal of leukocyte biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- An interpretable machine learning tool for rheumatoid arthritis screening: integrating novel cellular morphological parameters with routine blood count indices.Clinical rheumatology · 2026Article
- Altered neutrophil signalling linked to impaired chemotaxis and increased ROS and NET production in older people with frailty.Clinical and experimental immunology · 2026Article
- Network-based analysis identifies shared mechanisms between ischemic stroke and myocardial infarction and therapeutic ingredients of Buyang Huanwu Decoction.Frontiers in genetics · 2026Article
- The Zebrafish miR-183 Family Regulates Endoderm Convergence and Heart Development via S1Pr2 Signaling Pathway.Biomolecules · 2025Article
- Roles of Neutrophils in Autoimmune Diseases and Cancers.International journal of molecular sciences · 2025Review
- The small molecule inhibitor 3PO is a modulator of neutrophil metabolism, ROS production, and NET release.Clinical and experimental immunology · 2025Article
- Cytokine-induced transcriptional changes in human neutrophils reveal immune regulatory plasticity.Discovery immunology · 2025Article
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Authors and funding
10 authors.
Funding
Abstract
Neutrophils are innate immune cells that drive the progression of rheumatoid arthritis through the release of reactive oxygen species, neutrophil extracellular traps, and proteases that damage host tissues. Neutrophil activation is regulated, in part, by dynamic changes in gene expression. In this study, we have used RNAseq to measure the transcriptomes of neutrophils from people with severe, methotrexate-refractory rheumatoid arthritis and healthy controls. We identified a dynamic gene expression profile in people with severe rheumatoid arthritis. This is dominated by a type-I interferon-induced gene expression signature as well as activation of genes regulating neutrophil degranulation, neutrophil extracellular trap production, response to reactive oxygen species, and oxidative stress. While we did not detect significantly elevated levels of interferon-alpha in rheumatoid arthritis blood sera, we identified increased expression in rheumatoid arthritis neutrophils of miR-96-5p and miR-183-5p, which regulate activation of the interferon pathway as members of the miR-183C cluster. We also detected significantly elevated neutrophil extracellular trap debris in rheumatoid arthritis blood sera (P < 0.05). Using gene set variation analysis, we explored the heterogeneity of neutrophil gene expression in rheumatoid arthritis and identified subsets of patients with gene expression profiles reflecting enhanced neutrophil degranulation and cytotoxicity, tissue inflammation, or activation by interferons. Comparison with published single-cell RNAseq datasets identified rheumatoid arthritis transcriptomes where neutrophils were polarized by genes relating to early or late cell maturity, with significant genes in each polarized state being regulated by miR-146a-5p, miR-155-5p, miR-183-5p, or miR-96-5p. Overall, our study demonstrates the heterogeneity of the rheumatoid arthritis neutrophil transcriptome and proposes microRNA-driven mechanisms for regulating the activated neutrophil phenotype in rheumatoid arthritis.
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