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首页> 外文期刊>Cytokine >Differential effects of lactacystin on cytokine production in activated Jurkat cells and murine splenocytes.
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Differential effects of lactacystin on cytokine production in activated Jurkat cells and murine splenocytes.

机译:乳胞素对活化的Jurkat细胞和鼠脾细胞中细胞因子产生的差异作用。

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Previous studies have demonstrated that the proteasome inhibitor, lactacystin, suppresses cytokine production and induction of other inflammatory mediators by LPS-stimulated macrophages. The purpose of the present studies was to determine the effect of lactacystin upon the function of activated human Jurkat T cells and murine splenocytes. Lactacystin treatment suppressed interleukin (IL)-2, interferon (IFN)gamma, and IL-13 production similarly in both activated Jurkat cells and primary splenocytes. Interestingly, lactacystin produced differential effects on IL-4 transcription in the two models. While lactacystin inhibited IL-4 mRNA transcription in primary splenocytes, it induced IL-4 mRNA in a concentration-dependent manner in Jurkat cells. The increase in IL-4 mRNA levels by lactacystin did not correlate with increases in T(H2)-specific transcription factors, avian musculoaponeurotic fibrosarcoma AS42 oncogene homolog (c-maf) or GATA binding protein 3 (GATA-3). In addition, the binding of both GATA-3 and t-bet to their respective response elements was essentially unchanged by lactacystin treatment in both splenocytes and Jurkat T cells, suggesting the induction of IL-4 is due to other mechanisms. Collectively, the current studies suggest proteasomal activity has differential effects on IL-4 transcription in activated Jurkat cells and primary splenocytes.
机译:先前的研究表明,蛋白酶体抑制剂乳酸菌素可抑制LPS刺激的巨噬细胞产生的细胞因子并诱导其他炎症介质。本研究的目的是确定乳酸菌素对活化的人Jurkat T细胞和鼠脾细胞功能的影响。 Lactacystin处理在激活的Jurkat细胞和原代脾细胞中均抑制白介素(IL)-2,干扰素(IFN)γ和IL-13的产生。有趣的是,乳酸菌素在两种模型中对IL-4转录产生不同的作用。乳杆菌素抑制原代脾细胞中IL-4 mRNA的转录,但在Jurkat细胞中以浓度依赖的方式诱导IL-4 mRNA。乳酸菌素引起的IL-4 mRNA水平升高与T(H2)特异性转录因子,禽肌腱膜纤维肉瘤AS42癌基因同源物(c-maf)或GATA结合蛋白3(GATA-3)升高无关。另外,在脾细胞和Jurkat T细胞中,通过乳胞素处理,GATA-3和t-bet均与它们各自的响应元件结合基本上没有改变,这表明IL-4的诱导是由于其他机制引起的。总的来说,当前的研究表明蛋白酶体活性对活化的Jurkat细胞和原代脾细胞中的IL-4转录具有不同的影响。

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