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

Abstract

Several studies proved that microRNA (miRNA) originated from cells or body fluids can serve as disease-specific biomarkers in many diseases, including rheumatoid arthritis (RA). In this study, we investigated the effects of Janus Kinase (JAK) selective inhibitor—baricitinib treatment on Treg populations and Treg-derived miRNA in context of basic thrombotic parameters. Blood samples from healthy controls (HCs) and RA patients were used for Treg phenotyping and miRNA detection. Thrombotic parameters were investigated in citrated plasma of RA and HCs. KEGG pathways enrichment analysis of selected four miRNAs was performed using DIANA-mirPath databases to predict the interaction between selected miRNAs and their mRNA targets. Baricitinib treatment resulted in significant CD4⁺Foxp3⁺ Treg population decrease (4.6 ± 0.4 vs. 5.6 ± 0.4; p = 0.01) and was characteristic of good responders’ patient group. In this group, significantly lower expression of four miRNAs—miRNA-17, miRNA-142, miRNA-146, and miRNA-155—in comparison to moderate responders or HCs was noticed. The expression of all selected miRNA and miRNA-125 negatively correlated with antithrombin III level. KEGG analysis showed that levels of selected miRNA were strongly associated with four pathways regulating immunity and inflammation. We identified a panel of miRNA in Tregs that can serve as biomarkers of good response in baricitinib therapy.