【摘 要】
：
Heat shock response is a self-defense mechanism for protection of cells and organisms from a wide range of harmful stressors. Recent studies revealed that it is
【机 构】
：
Shanghai Institute of Biochemistry and Cell Biology,Department of Cell Biology
【基金项目】
：
国家重点基础研究发展计划(973计划);中国科学院科研项目
论文部分内容阅读
Heat shock response is a self-defense mechanism for protection of cells and organisms from a wide range of harmful stressors. Recent studies revealed that it is involved in the regulation of cytokines expression. IL-18 is an important cytokine in mediating immune response. We studied LPS-induced IL-18 expression in heat shock treated RAW264.7 murine macrophages. Our results show that the heat shock response significantly inhibited the expression of LPS-induced pro-inflammatory cytokine IL-18. Further research on the down-regulation mechanism shows that this inhibitory effect is correlated to the great suppression of the binding activity of AP-1, which is a transcription factor binding to the promoter of IL-18 (-1120 to -1083) and regulates the transcription of IL-18. Meanwhile, we observed that the phosphorylation of JNK, which is AP-1 upstream kinase, was greatly decreased. These results confirmed that the down-regulation effect on IL-18 production in heat shock response is related to the suppression of the JNK/AP-1 signaling pathway.
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