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Histone deacetylase inhibitors decrease the antigen presenting activity of murine bone marrow derived dendritic cells.

机译:组蛋白脱乙酰基酶抑制剂降低了小鼠骨髓衍生的树突状细胞的抗原呈递活性。

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Once activated by infected pathogens, dendritic cells (DCs) undergo activation and release inflammatory mediators responsible for the signs of inflammation. Our aim was to elucidate whether histone deacetylase inhibitors (HDACIs), trichostatine-A (TSA), scriptaid (ST) and sodium butylate (SB) regulate the inflammatory response of DCs. Pre-treatment with TSA and ST reduced the syngeneic and allogeneic-antigen presenting activity of LPS-stimulated DCs in a dose dependent manner to statistical significance. SB also reduced the antigen presenting activity of DCs, but not significantly. HDACIs mediate their effects through the modulation of DC maturation and pre-treatment of the DCs with TSA or ST prior to treatment with LPS reduced the expressions of DC mature markers to the level of immature dendritic cells (iDCs). Moreover, TSA and ST reduced the IL-2 production from LPS-stimulated mature DCs. Our results suggest that HDACIs may actively modulate the DC-induced inflammatory response through inhibition of phenotypical or functional maturation.
机译:一旦被感染的病原体激活,树突状细胞(DC)就会被激活并释放引起炎症迹象的炎症介质。我们的目的是阐明组蛋白脱乙酰基酶抑制剂(HDACIs),曲古他汀A(TSA),scriptaid(ST)和丁酸钠(SB)是否调节DC的炎症反应。用TSA和ST预处理以剂量依赖性方式降低了LPS刺激的DC的同基因和同种异体抗原呈递活性,具有统计学意义。 SB还降低了DC的抗原呈递活性,但没有明显降低。 HDACI通过调节DC成熟和在用LPS处理之前用TSA或ST预处理DC来介导其作用,从而将DC成熟标记的表达降低到未成熟树突状细胞(iDC)的水平。此外,TSA和ST减少了LPS刺激的成熟DC产生的IL-2。我们的结果表明,HDACIs可能通过抑制表型或功能性成熟来主动调节DC诱导的炎症反应。

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