中文摘要：

利用重组PCR的方法，克隆并构建MyD88和MyD88aa155-171功能区缺失（MyD88A155．171）载体，转染免疫相关细胞并筛选获得稳定细胞系。报告基因实验结果显示MyD88MyD88△155-171功能区缺失能够抑制转录因子NF—kB和AP-1的活性，在不同Toll样受体（TLR）配体刺激后，转染MyD88A155—171的细胞表面分子的表达低于MyD88正常表达的细胞，并且抑制表面分子CD86和B7H1在TLR配体刺激后的上调。同时，多细胞因子分析系统的检测结果表明，给予TLR配体刺激之后，MyD88^-/-树突细胞表达低水平的细胞因子，转染MyD88可以使细胞因子表达明显增加，而仅表达MyD88A155-171可以明显影响IL—12，IFN-γ的表达。以上结果表明MyD88功能区缺失影响免疫相关细胞表面分子和细胞因子的表达及Toll样受体信号的传递．其在细胞内信号系统的具体作用机制还需进一步证实。

英文摘要：

Myeloid differentiation factor MyD88 is a critical adaptor molecule that integrates and transduces intracellular signals in inducing the differentiation of dendritic cells （DCs）. The domain regions within MyD88 was searched ,it could potentially affect the function of dendritic cells and found that MyD88 aa155-171 motif not only regulate the activity of transcription factor NF-kB, but also control the production of cytokines and expression of costimulatory molecules. Indeed, aa155 -171 motif deleted type MyD88 （ MyD88A155 -171 ） transfected RAW264.7 cells exhibited the reduced NF-kB and AP-1 activity and interrupted the expression of CD86 and B7H1. Meanwhile, lower level expression of cytokines such as IL-12,IFN-γ were also observed by means of cytokine array in MyD88^-/- DC trasfected with MyD88A155-171 as compared to the MyD88 transfected cells. Thus, aa155-171 motif inside MyD88 could affect the expression of costimulatory molecules, production of cytokines and transduction of Toll like receptor signal pathway, suggesting that this motif may play an important role in regulating responses of innate immune system.