DC通过调节T细胞亚群的分化，在维持免疫耐受、启动免疫反应中起着关键性的作用。在静息状态下，非成熟和耐受性DC通过合成IL-10，TGF-b和维甲酸等分子，促进调节性T细胞的发育，维持免疫耐受。在病菌感染时，TLR等天然免疫信号通路被激活，导致DC的活化，启动免疫反应。活化的DC上调共激活分子，表达IL-12等细胞因子，促进Th1和杀伤性T细胞的分化，启动宿主防御功能。我们和其他实验室的研究表明TLR等天然免疫信号通路还能激活mTOR，上调SREBP的表达，在DC中促进脂肪酸的合成，但mTOR-SREBP调节的脂代谢在DC活化和DC介导的免疫耐受、抗感染免疫中的作用还不清楚。因此本研究试图利用在DC中特异性敲除TSC1-mTOR和SREBP的小鼠模型，探究脂代谢在DC活化，自身免疫性疾病和抗感染中的作用，并阐明其作用的分子机制。该研究的结果有望为治疗自身免疫性和感染性疾病提供新思路。

By guiding the differentiation of distinct T cell subsets,DCs play a critical role in maintaining the immune tolerance and the initiation of adaptive immune responses.In resting state,immature or tolerogenic DCs are responsible for Treg differentiation through their high expression of IL-10,TGF-b and Retinoic acid.In contrast,engaging innate immune receptors such as TLRs by pathogens can lead to the activation of DCs.In turn, TLR-activated DCs upregulate the expression of co-stimulatory molecules as well as a myriad of cytokines including IL-12,whereby promote the differentiation of Th1 and CTL responses.Interestingly, we and the others have recently found that TLR signaling can also activate mTOR, upregulating SREBP expression and the elevation of lipid synthesis in DCs.However, the role of mTOR-SREBP-regulated lipid synthesis in DC activation as well as DC-mediated immune tolerance and pathogen-specific adaptive immunity remain unclear.In this study, we attempt to generate unique mouse strains which are deficient in either TSC1,mTOR or SREBP specifically in DC lineage, whereby study the role of lipid metabolism in DC activation and function, particularly in the settings of autoimmunity and viral infection.It is expected that our study may provide new insights on how to treat autoimmune and infectious diseases by manipulating the lipid metabolism pathways.