ArticleArthritis research & therapy2018
Aberrant expression of interleukin-23-regulated miRNAs in T cells from patients with ankylosing spondylitis.
Article in Arthritis research & therapy, 2018. 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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7 citing papers in PubMed, 16 citations in OpenAlex.
- Immune Regulatory Endotypes Defined by TRIM-Dependent Ubiquitin Signaling and IFN-NF-κB Network Activity in Ankylosing Spondylitis.International journal of molecular sciences · 2026Article
- Interpreting the Function of the IL-23/IL-17 Axis through Bioinformatics.Endocrine, metabolic & immune disorders drug targets · 2025Review
- Dysregulated Non-Coding RNA Expression in T Cells from Patients with Ankylosing Spondylitis Contributes to Its Immunopathogenesis.Biomedicines · 2024Review
- Analysis of genetically independent phenotypes identifies shared genetic factors associated with chronic musculoskeletal pain conditions.Communications biology · 2020Article
- The Neat Dance of COVID-19: NEAT1, DANCR, and Co-Modulated Cholinergic RNAs Link to Inflammation.Frontiers in immunology · 2020Article
- Differential Expression Profiles of the Transcriptome and miRNA Interactome in Synovial Fibroblasts of Rheumatoid Arthritis Revealed by Next Generation Sequencing.Diagnostics (Basel, Switzerland) · 2019Article
- Prostaglandin receptor EP4 expression by Th17 cells is associated with high disease activity in ankylosing spondylitis.Arthritis research & therapy · 2019Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundInterleukin (IL)-23 can facilitate the differentiation of IL-17-producing helper T cells (Th17). The IL-23/IL-17 axis is known to play a key role in the immunopathogenesis of ankylosing spondylitis (AS). We hypothesized that the expression of microRNAs (miRNAs, miRs) would be regulated by IL-23 and that these miRNAs could participate in the immunopathogenesis of AS.
methodsExpression profiles of human miRNAs in K562 cells, cultured in the presence or absence of IL-23 for 3 days, were analyzed by microarray. Potentially aberrantly expressed miRNAs were validated using T-cell samples from 24 patients with AS and 16 control subjects. Next-generation sequencing (NGS) was conducted to search for gene expression and biological functions regulated by specific miRNAs in the IL-23-mediated signaling pathway.
resultsInitial analysis revealed that the expression levels of 12 miRNAs were significantly higher, whereas those of 4 miRNAs were significantly lower, in K562 cells after coculture with IL-23 for 3 days. Among these IL-23-regulated miRNAs, the expression levels of miR-29b-1-5p, miR-4449, miR-211-3p, miR-1914-3p, and miR-7114-5p were found to be higher in AS T cells. The transfection of miR-29b-1-5p mimic suppressed IL-23-mediated signal transducer and activator of transcription 3 (STAT3) phosphorylation in K562 cells. After NGS analysis and validation, we found that miR-29b-1-5p upregulated the expression of angiogenin, which was also upregulated in K562 cells after coculture with IL-23. Increased expression of miR-29b-1-5p or miR-211-3p could enhance interferon-γ expression.
conclusionsAmong the miRNAs regulated by IL-23, expression levels of five miRNAs were increased in T cells from patients with AS. The transfection of miR-29b-1-5p mimic could inhibit the IL-23-mediated STAT3 phosphorylation and might play a role in negative feedback control in the immunopathogenesis of AS.
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