The genes affected by Triptolide in activated mouse primary T cells

Triptolide possesses immunosuppressive activity and its efficacy is commonly believed to be related to the suppression of T cells. However, the underlying mechanism is still not well documented and most of the previous study adopted tumor cell lines of immune system as model cells in mechanism research, these cells’ signal transduction pathway can not reflect the real situation of immune system. In this study, we investigated the immunosuppressive mechanism of triptolide on T cell activation and proliferation using mouse primary T lymphocytes. These effects were analyzed along with activation of the TCR and AP-1 pathway. We used microarrays to detail the global programme of gene expression underlying stimulation and triptolide treatment. Mouse primary T cells stimulated with anti-CD3/CD28 antibodies treated with triptolide or not treated with triptolide were selected for RNA extraction and hybridization on Affymetrix microarrays.

雷公藤内酯醇（Triptolide）具有免疫抑制活性，其疗效通常被认为与T细胞的抑制作用密切相关。然而，其具体的潜在分子机制尚未得到充分阐明。既往开展的相关机制研究多采用免疫系统来源的肿瘤细胞系作为模型细胞，但此类细胞的信号转导通路无法真实反映体内免疫系统的生理状态。本研究以小鼠原代T淋巴细胞为实验模型，探究雷公藤内酯醇对T细胞活化与增殖的免疫抑制机制，并同步分析T细胞受体（TCR）与激活蛋白1（AP-1）通路的激活状态。我们通过基因芯片（microarrays）技术，详细解析了T细胞在受刺激并经雷公藤内酯醇处理后的全局基因表达特征。本研究选取经抗CD3/CD28抗体刺激、并分别施加雷公藤内酯醇处理与未处理的小鼠原代T细胞，提取其总RNA后在Affymetrix基因芯片上完成杂交实验。