Abstract
Oxysterol like 27-hydroxycholesterol (27OHChol) has been reported to induce differentiation of monocytic cells into a mature dendritic cell phenotype. We examined whether dexamethasone (Dx) affects 27OHChol-induced differentiation using THP-1 cells. Treatment of monocytic cells with Dx resulted in almost complete inhibition of transcription and surface expression of CD80, CD83, and CD88 induced by 27OHChol. Elevated surface levels of MHC class I and II molecules induced by 27OHChol were reduced to basal levels by treatment with Dx. A decreased endocytosis ability caused by 27OHChol was recovered by Dx. We also examined effects of Dx on expression of CD molecules involved in atherosclerosis. Increased levels of surface protein and transcription of CD105, CD137, and CD166 by treatment with 27OHChol were significantly inhibited by cotreatment with Dx. These results indicate that Dx inhibits 27OHChol-induced differentiation of monocytic cells into a mature dendritic cell phenotype and expression of CD molecules whose levels are associated with atherosclerosis. In addition, we examined phosphorylation of AKT induced by 27OHChol and effect of Dx, where cotreatment with Dx inhibited the phosphorylation of AKT. The current study reports that Dx regulates oxysterol-mediated dendritic cell differentiation of monocytic cells.
Highlights
Dexamethasone (Dx), a glucocorticoid, is widely used in treatment of chronic inflammatory and immunological diseases because it is a potent immune-suppressive and antiinflammatory drug [1, 2]
We determined expression of mature DCs (mDCs) markers to examine whether Dx affects differentiation of monocytic cells induced by 27OHChol
CD80, CD83, and CD88, and addition of Dx resulted in their attenuated transcription, as determined by real-time
Summary
Dexamethasone (Dx), a glucocorticoid, is widely used in treatment of chronic inflammatory and immunological diseases because it is a potent immune-suppressive and antiinflammatory drug [1, 2]. Dx inhibits secretion of inflammatory mediators [3] and Th1 type immune response [4]. Dx alters function of monocyte-derived dendritic cells (MoDCs) from cord blood [6] and inhibits maturation of dendritic cells (DCs) by redirecting differentiation of a subset of cells [7]. Dx inhibits the antigen presentation of DCs [8]. These reports indicate that Dx affects immunological responses by regulating differentiation and function of DCs
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