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热休克反应(HSR)是机体或细胞保护自身免受一系列有害刺激的自我保护性反应, 近年来的研究表明它还参与了细胞因子的表达调节. IL-18是调节免疫反应的一个重要的细胞因子. 研究了小鼠巨噬细胞(RAW264.7)中HSR对脂多糖(LPS)诱导的IL-18表达的效应, 结果表明, HSR强烈抑制了LPS引起的IL-18的mRNA的转录和蛋白分泌. 进一步对这一下调效应机制的研究表明, 在热休克细胞中, 介导IL-18表达的转录因子AP-1与IL-18启动子区域(-1120 ~ -1083)的DNA序列结合活性明显下降, AP-1上游激酶JNK的磷酸化水平也显著降低. 上述这些研究结果提示, HSR对IL-18表达的下调效应与JNK/AP-1信号通路的抑制密切相关.
Heat shock response (HSR) is a self-protective reaction in which the body or cell protect itself from a series of unpleasant stimuli, and recent studies have shown that it is also involved in the regulation of cytokine expression. IL-18 is an important regulator of the immune response Cytokines The effect of HSR on lipopolysaccharide (LPS) -induced IL-18 expression in mouse macrophages (RAW264.7) was studied and showed that HSR strongly inhibited the transcription of IL-18 mRNA induced by LPS and Protein secretion.Studies on this down-regulation mechanism further show that in heat-shocked cells, the transcription factor AP-1 that mediates IL-18 expression binds to the DNA sequence of the IL-18 promoter region (-1120 -1083) And the phosphorylation of JNK, an upstream kinase of AP-1, was significantly decreased.These results suggest that the down-regulation effect of HSR on IL-18 expression is closely related to the inhibition of JNK / AP-1 signaling pathway.