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DEXAMETHASONE IN VITRO, AND PULSE-THERAPY WITH GLUCOCORTICOIDS IN VIVO INDUCE TOLEROGENIC PHENOTYPE OF DENDRITIC CELLS IN PATIENTS WITH RHEUMATOID ARTHRITIS


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Abstract

Dendritic cells (DCs) along with stimulatory activity can exert tolerogenic effect and suppress the functions of autoreactive T-lymphocytes. Therefore, the enhancement of DC tolerogenic properties is considered as a new strategy for rheumatoid arthritis (RA) treatment. The aim of the study is to examine the in vitro effect of dexamethasone on the stimulatory activity of interferon-alpha-induced dendritic cells (IFN-DCs) in auto- and allo-MLC and to evaluate the in vivo effect of high-dose methylprednisolone pulse-therapy on IFN-DCs functions in RA patients. It has been shown that dexamethasone induces the tolerogenic phenotype of patient’s monocyte-derived IFN-DCs which is manifested in the ability of dexamethasone-modified DCs to suppress T-cell proliferation and cytokine production in auto-MLC. In addition to that, the significant decrease of TNF-α/IL-10 and IFN-γ/IL-4 ratios indicates a more pronounced suppression of Th1/pro-inflammatory cytokines production and a shift towards Th2 response. The tolerogenic effect of glucocorticoids in vivo is manifested by marked decrease of IFN-DCs stimulatory ability after pulse-therapy with methylprednisolone. The revealed relationship (Rs= -0,71; p=0,02) between low IFN-DC stimulatory activity and enhanced level of CD14+CD16++ cells among blood monocytes suggests that the effect of glucocorticoids in vivo may be associated with the alteration of circulating monocyte’s subsets following pulse-therapy.


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