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<p>Rheumatoid arthritis (RA) is a chronic autoimmune disease in which long non-coding RNAs (lncRNAs) may contribute to immune dysregulation, but their regulation in circulating immune cells remains incompletely characterized. We measured the expression of four small nucleolar RNA host genes (SNHG1, SNHG3, SNHG4 and SNHG5) in peripheral blood mononuclear cells from 44 patients with RA and 20 healthy controls and examined their relationships with disease activity and autoantibody status. SNHG4, SNHG3, and SNHG1 were significantly lower in RA, whereas SNHG5 did not differ between groups. Reduced SNHG4 and SNHG1 were most pronounced in clinically active RA and in anti-citrullinated protein antibody–positive disease, and were observed in both rheumatoid factor–positive and rheumatoid factor–negative subgroups. Across patients, associations between SNHG levels and standard clinical or laboratory measures of disease activity were weak. These findings support compartment-specific regulation of SNHG lncRNAs in RA and suggest that SNHG1 and SNHG4 may contribute to future candidate molecules for molecular phenotyping. Larger, longitudinal studies integrating immune-cell subsets and joint tissue are needed to confirm clinical utility and clarify mechanisms.</p>

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Regulation of SNHG1, SNHG3, SNHG4 and SNHG5 in peripheral blood mononuclear cells in rheumatoid arthritis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月28日

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  • Dominika Podgórska,
  • Marek Cieśla,
  • Joanna Paśko,
  • Bogdan Kolarz

摘要

Rheumatoid arthritis (RA) is a chronic autoimmune disease in which long non-coding RNAs (lncRNAs) may contribute to immune dysregulation, but their regulation in circulating immune cells remains incompletely characterized. We measured the expression of four small nucleolar RNA host genes (SNHG1, SNHG3, SNHG4 and SNHG5) in peripheral blood mononuclear cells from 44 patients with RA and 20 healthy controls and examined their relationships with disease activity and autoantibody status. SNHG4, SNHG3, and SNHG1 were significantly lower in RA, whereas SNHG5 did not differ between groups. Reduced SNHG4 and SNHG1 were most pronounced in clinically active RA and in anti-citrullinated protein antibody–positive disease, and were observed in both rheumatoid factor–positive and rheumatoid factor–negative subgroups. Across patients, associations between SNHG levels and standard clinical or laboratory measures of disease activity were weak. These findings support compartment-specific regulation of SNHG lncRNAs in RA and suggest that SNHG1 and SNHG4 may contribute to future candidate molecules for molecular phenotyping. Larger, longitudinal studies integrating immune-cell subsets and joint tissue are needed to confirm clinical utility and clarify mechanisms.