POS0673 TOLEROGENIC DENDRITIC CELLS IN RHEUMATOID ARTHRITIS PATIENTS: NEWS AND PROMISES

Background: Dendritic cells (DCs) are known to contribute the pathogenesis of rheumatoid arthritis (RA) through presentation cartilage glycoprotein, production proinflammatory cytokines and activation Th1/Th17 responses. Along with stimulating activity, DCs may exhibit suppressive functions via capacity induce T cell apoptosis/anergy generate regulatory cells. Since these have potential control autoreactive T-lymphocytes, enhancing tolerogenic properties seems be a new important strategy in treatment RA. Dexamethasone is widely used clinical practice can as substance. Therefore, generated presence dexamethasone great interests. Objectives: The aim our study describe DCs, patients RA their influence on autologous T-cells. Methods: Sixty five high moderate activity disease were recruited this study. All follow ACR/EULAR criteria (2010). studies performed after receiving informed consent. received conventional synthetic DMARDs. from blood monocytes culturing for 5 days GM-CSF IFN-α (dexDCS), applied third day. LPS maturation stimuli was added fourth expression CD14, CD83, HLA-DR, TLR-2 surface measured by flow cytometry. evaluated measuring cytokine allostimulatory mixed lymphocyte culture. Mature absence control. Results: We revealed that dexDCs characterized enhanced CD14+cells decreased number CD83+cells but percent HLA-DR+cells constant (about 85). DexDCs show seen molecule (75%vs51%, p=0.05 compared control). also marked prominent increase TNFα/IL-10 ratio contrast (0.59 vs 1.8, p=0.03). suppressed proliferation allogenic T-cells (2005 7980 cpm, p=0.0002). To assess stability DC proinfflamatory micro-environment assessing stimulatory then cultivated one more. stimulation incubation not (4692 6053 p=0.7). Also earlier we showed possibility induse apoptosis T-cells, CD4+IL10+Tr1 possession antigen-specific suppression. Conclusion: data obtained indicate main features stable inflammatory environment proves arthritis. Disclosure Interests: None declared