树突细胞通过激活、诱导初始T细胞而成为调节免疫反应和免疫耐受的中心环节。iDC活化转变为mDC可刺激淋巴细胞增殖，分泌炎性因子。因此，抑制iDC细胞的活化可达到缓解RA的目的。TLR是体内活化iDC的关键信号，阻断TLR可抑制iDC的活化。在前期研究中，我们发现TRAF6是TLR通路中的关键接头分子。因此，我们提出假设：TRAF6可能是体内活化iDC的关键信号分子，其在调控iDC成熟中可发挥"总开关"作用。为证实这一假说, 我们拟建立胶原诱导性关节炎大鼠模型、体外诱导培养骨髓来源DCs，以流式细胞术和ELISA检测DCs的表面标志与IL-12分泌;Western blotting 和RT-PCR法检测DCs的TRAF6蛋白水平及mRNA的表达；RNAi技术研究沉默TRAF6基因表达是否能抑制iDC活化，证实TRAF6作为"分子开关"抑制iDC成熟而重建RA免疫耐受，为RA寻求新的治疗靶点。

Dendritic cells through the activation, induced initial T cell and become the central link to adjust immune response and the immune tolerance. IDC activation into mDC can stimulate lymphocyte proliferation, secrete proinflammatory cytokines. Therefore, inhibiting iDC cell activation will achieve the purpose of alleviating RA. TLR is the key signal of activating iDC in vivo, blocking TLR can influence the activation of the iDC. In the previous study, we found that TRAF6 is the key receptor protein in TLR pathway. Therefore, we put forward assumption: TRAF6 may be the key signal molecules activating iDC，it may play the "main switch" effect in the regulation of iDC mature. To prove this hypothesis, we will develop a rats type II collagen-induced arthritis model, induce and cultivate marrow-derived DC in vitro . The surface mark of the DC is detected by flow cytometry and the secretion of IL-12 is measured by ELISA;The levels of TRAF6 protein in DC and the expression of the mRNA are respectively detected by Western blotting and RT-PCR ; Through RNAi technology , we research that silence TRAF6 gene expression whether can inhibite of the iDC activation, prove that TRAF6 as "molecular switch" inhibiting the mature of iDC and reconstructing RA immune tolerance,and seek new therapeutic targets.