Significance of miRNA Profile of Regulatory T Cells (Tregs) After Baricitinib Treatment in Rheumatoid Arthritis

Magdalena Massalska1, Anna Felis-Giemza2, Patrycja Gardias1

  • 1Department of Pathophysiology and Immunology, National Institute of Geriatrics, Rheumatology and Rehabilitation, Warsaw, Poland.

PubMed

Insights

MicroRNAs (miRNAs) from regulatory T cells (Tregs) show promise as biomarkers for baricitinib treatment response in rheumatoid arthritis (RA). Lower levels of specific miRNAs indicate a good response to JAK inhibitor therapy.

Area of Science:

  • Immunology
  • Molecular Biology
  • Rheumatology

Background:

  • MicroRNAs (miRNAs) are emerging as disease-specific biomarkers in various conditions, including rheumatoid arthritis (RA).
  • Regulatory T cells (Tregs) play a crucial role in immune regulation and are implicated in autoimmune diseases like RA.

Purpose of the Study:

  • To investigate the impact of Janus Kinase (JAK) selective inhibitor-baricitinib on Treg populations and their derived miRNAs in RA patients.
  • To identify potential miRNA biomarkers associated with baricitinib treatment response and thrombotic parameters in RA.

Main Methods:

  • Analysis of Treg populations and miRNA expression in blood samples from healthy controls (HCs) and RA patients.
  • Thrombotic parameter assessment in RA and HCs.
  • KEGG pathway enrichment analysis to predict miRNA-mRNA target interactions.

Main Results:

  • Baricitinib treatment led to a significant decrease in CD4+Foxp3+ Treg populations, characteristic of good responders.
  • Good responders exhibited significantly lower expression of miR-17, miR-142, miR-146, and miR-155 compared to moderate responders or HCs.
  • Selected miRNA expression negatively correlated with antithrombin III levels and was associated with immune and inflammation pathways.

Conclusions:

  • A panel of miRNAs within Tregs can serve as biomarkers for predicting a good response to baricitinib therapy in RA.
  • These miRNAs are linked to pathways regulating immunity and inflammation, highlighting their role in RA pathogenesis and treatment response.

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