Background: Dendritic cells (DCs) are known to contribute to the pathogenesis of autoimmune diseases through presentation of cartilage glycoprotein, production of proinflammatory cytokines and activation of Th1/Th17 responses. DCs are a heterogeneous population and can be divided into groups: myeloid (mDCs) and plasmacytoid (pDCs). DCs can induce both immune response and tolerance.

Objectives: The study is aimed at investigating the subpopulations of peripheral blood DCs (myeloid and plasmacytoid) in patients with rheumatoid arthritis (RA) and axial spondyloarthritis (axSpa) under disease-modifying antirheumatic drugs (DMARDs) treatment as a target of pathogenic therapy.

Methods: There are thirty patients were included in the study. Twenty patients with early RA (ACR/EULAR criteria, 2010, duration of the disease up to 12 months,) and ten patients with axSpa (ASAS criteria) were recruited. RA patients received methotrexate, leflunomide, sulfasalazine or their combination. All patients received NSAID in combination with conventional synthetic DMARDs. Analysis of the content of the B-lymphocytes, myeloid and plasmacytoid DCs was carried out by flow cytometry. B-lymphocytes, subtypes of peripheral blood DCs were characterized by the following phenotypes: myeloid DCs (CD3-CD14-CD19-HLA-DR + CD11c + CD123-), plasmacytoid DCs (CD3-CD14-CD19-HLA-DR + CD11c-CD123 +), B-lymphocytes (CD19 +). Analyses were performed before treatment and 6 months later.

Results: RA patients were characterized by high activity of the disease (DAS28=5.46). At the beginning we revealed significant increasing of the population of myeloid DCs (1.6%) and B-lymphocytes (5.4%). No significant differences were observed in the number of plasmacytoid DCs. After 6 months of treatment, most of the patients had a decrease in the activity of the disease (DAS28=3.5vs5.46, p=0.05, n=12) coupled with a significant decrease mDCs (0.85 vs1.6%, p=0.03) and B-cells (4.2 vs 5.4%, p=0.05). In the remaining patients (n=8), there was no clinically significant improvement (DAS28=4.96) or differences in mDCs (1.45 vs1.6%) and B-cells (5.0vs5.4%). Six months later, there was a decrease in ASDAS activity among axSpa patients (2.56 vs 2.09). We were revealed no differences in amount in mDCs between RA and axSpa patients (1.4 vs 1.6%). After 6 month of investigation we detected decreasing mDCs (1.4 vs 0.9%, p=0.05). We have also found a decrease in B lymphocytes among axSpa patients (5.1 vs 4.1%) that is consistent with some authors’ data on B lymphocytes in spondyloarthritis pathogenesis.

Conclusion: Reduction in the number of DCs in the context of treatment combined with reduced activity of diseases confirm the role of DCs in the pathogenesis of autoimmune diseases. In addition, probably being a target of pathogenetic therapy, they can serve as a marker of a good clinical response to the therapy.

Disclosure of Interests: None declared