Background: Dendritic cells (DCs) are known to contribute to the pathogenesis of rheumatoid arthritis (RA) 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: To investigate the subpopulations of peripheral blood DCs (myeloid and plasmacytoid) in patients with early RA as a predictor of responsibility to disease-modifying antirheumatic drugs (DMARDs) treatment.

Methods: Fifty two patients with early RA (duration of the disease up to 12 months) were included in the study. All patients fullfield ACR/EULAR criteria (2010) and received methotrexate, leflunomide, sulfasalazine or their combination. Fifty five patients with osteoarthritis (OA) used as a control group. 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 after 3 and 6 months.

Results: Patients with early RA are characterized by significant evaluation of the population of myeloid DCs in comparison of patients with osteoarthritis (26.6% vs 23.5, p=0.0007). Furthermore, the difference was found in the number of cells with the phenotype B-lymphocytes: 5.4% vs 3%, p = 0.0005). No significant differences were observed in the number of plasmocytoid DCs. After 3 and 6 month of observation we detected reducing amount of myeloid DCs 26.6% vs 21.1% vs 18.4% respectively. Also we revealed reducing B-cells in treatment (5.4% vs 3 % vs 2%). Disease activity according to DAS28 droped to low (4.32 to3.06, p=0.03). We also revealed a reliable negative correlation between both the activity of the disease and the B- cells (rS=-0.4, p=0.05, n=52) and myeloid DCS (rS=-0.6, p=0.0004, n=52). A reducing of the immune cells during the DMARDS therapy suggests that they are an attractive marker for good clinical response to therapy.

Conclusion: The data obtained confirm the determining role of myeloid DC and B lymphocytes in maintaining systemic inflammation in rheumatoid arthritis. In addition, these cells are a target of DMARDs therapy and a predictor of a good clinical response.

Disclosure of Interests: None declared