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首页> 外文期刊>FEBS letters. >Oxysterol represses high-affinity IgE receptor-stimulated mast cell activation in Liver X receptor-dependent and -independent manners.
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Oxysterol represses high-affinity IgE receptor-stimulated mast cell activation in Liver X receptor-dependent and -independent manners.

机译:氧固醇以肝脏X受体依赖性和非依赖性方式抑制高亲和力IgE受体刺激的肥大细胞活化。

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摘要

Oxysterols activating liver X receptors (LXRs) repress expression of pro-inflammatory genes and have anti-inflammatory effects. Here, we show for the first time that bone marrow-derived murine mast cells (BMMCs) predominantly express LXRbeta. 25-hydroxycholesterol, a representative LXR activating oxysterol, suppressed IL-6 production and degranulation response in BMMCs following engagement of high-affinity IgE receptor (FcepsilonRI). Interestingly, 25-hydroxycholesterol reduced cell-surface FcepsilonRI expression by inhibiting assembly of FcepsilonRIalpha and FcepsilonRIbeta. We demonstrate that LXR activation was involved in the suppression of IL-6 production in BMMCs, but that reduced FcepsilonRI expression and degranulation response was mediated in an LXR-independent manner.
机译:激活肝脏X受体(LXR)的氧甾醇会抑制促炎基因的表达并具有抗炎作用。在这里,我们首次展示了骨髓来源的鼠肥大细胞(BMMC)主要表达LXRbeta。高亲和力IgE受体(FcepsilonRI)参与后,代表LXR活化氧固醇的25-羟基胆固醇抑制了BMMC中IL-6的产生和脱粒反应。有趣的是,25-羟基胆固醇通过抑制FcepsilonRIalpha和FcepsilonRIbeta的装配来降低细胞表面FcepsilonRI的表达。我们证明LXR激活参与抑制BMMC中IL-6的产生,但是FcepsilonRI的表达减少和脱粒反应以LXR独立的方式介导。

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