白色念珠菌由酵母相向菌丝相转换会引起机体抗原递呈细胞中TLR2/6介导的IL-10表达上调，并诱导机体保护性免疫应答偏倚；C型凝集素样受体DC-SIGN可识别念珠菌细胞壁中α-甘露糖并通过Raf-1途径诱导多种TLR介导IL-10表达上调。我们推测：念珠菌向菌丝相转换中，以DC－SIGN为免疫识别靶点并通过Raf-1途径诱导TLR2、4介导IL－10等抗炎因子表达上调，导致CD4+Th0细胞向Th2细胞分化。.本课题拟采用TLR信号阻断、RNAi和染色质免疫共沉淀等技术分析：念珠菌向菌丝相转换过程中是否通过DC-SIGN/Raf-1途径负向调控TLR2、4介导的炎性因子并诱导共培养的CD4+Th0细胞分化的偏倚；并通过动物实验进一步验证DC-SIGN/Raf-1的阻断对小鼠树突状细胞介导的保护性免疫应答的影响，从而为DC-SIGN能否作为免疫治疗念珠菌病的有效靶位提供实验室依据。

The transition of Candida albicans (C. albicans) from yeast phase into mycelial phase will induce the up-regulation of IL-10 expression on human dentritic cells (DCs) in a manner dependent on TLR2/6 signalling pathway, and trigger the bias of protective immunity against C. albicans. Notiveably, upon recognition of α-mannose moiety on the cell wall of C. albicans by DC-SIGN, a C-type lectin receptor, the associated Raf-1 signalling pathway is activated and consequently induce the up-regulation of IL-10 mediated by TLRs. Accordingly, we infer that DC-SIGN may be the target of C. albicans during the transition into the mycelial phase, which will induce the up-regulation of anti-inflammatory cytokines including IL-10 mediated by TLR2 and TLR4, and facilitates the development of initial CD4+ helper T lymphocytes (Th0) into the Th2 cells..In this project, the blockage of TLRs associated signalling pathway, RNAi and Chromatin Immunoprecipitation (CHIP) techniques will be introduced to analyze whether the expression of inflammatory cytokines mediated by TLR2 and TLR4 is down-regulated in a DC-SIGN/Raf-1 dependent manner, and therefore, whether the negetively biased development of co-cultured CD4+ helper T lymphocytes is triggered. Furthermore, the animal experiments are designed to assess the effects of DC-SIGN/Raf-1 blockage on the protective immunity mediated by murine DCs, and accordingly, we hope to provide the assistance for the hyphothesis that DC-SIGN might be the effective target for the immunological therapy of candidiasis.