前期研究表明Treg/Th17及相关细胞因子在斑块状和点滴状银屑病间存在差异，Treg对Th17抑制减弱在银屑病发生和维持中起关键作用。已有研究表明NF-κB调控促炎（IL-1β和IL-6）和抗炎细胞因子（p53）的产生，Stat3可抑制NF-κB诱导基因的表达，组蛋白去乙酰化酶Sirt1与Foxp3共定位于胞核，可降低Treg细胞的功能，但对Treg产生IL-17及是否通过Sirt1-Stat3-NF-κB-p53通路调控Th17的分化及效应功能尚待阐明。本研究首先检测斑块状和点滴状银屑病中Sirt1在Treg和Th17上的表达及对Treg抑制Th17的影响；然后分析Sirt1抑制剂对 Treg/Th17产生IL-17及对Th17与角质形成细胞相互作用的影响，并分析NF-κB、Stat3和p53磷酸化和乙酰化水平的改变。以探讨Sirt1在银屑病中的免疫调节机制，为银屑病治疗引入新的靶点。

Previous study revealed that Treg/Th17 and related cytokines were shown differently between guttate and plaque psoriasis. The weakened inhibitory function of Treg for Th17 plays a essential role in the development and maintenance of psoriasis.It has been shown that NF-κB regulates the production of proinflammatory (IL-1β and IL-6) and anti-inflammatory (p53) cytokines. Stat3 inhibits the expression of NF-κB-induced genes. Sirt1, Class Ⅲ histone/protein deacetylase, has been shown their co-localization with Foxp3 in the nucleus, and reduced the function of Treg. However, Whether Sirt1 controls the differentiation and effective function of Th17 by the Sirt1-Stat3-NF-κB-p53 pathway and influences Treg producing IL -17 has to be elucidated. In this study we will firstly detect the expression of Sirt1 on Treg and Th17 and the impact of Sirt1 on the inhibitory function of Treg for Th17 in guttate and plaque psoriasis. Secondly, we will analyze the effect of Sirt1 inhibitor on the Treg/Th17 produing IL-17 and the interaction between Th17 and keratinocyte, and analyze the alteration of phosphorylated and acetylated NF-κB, Stat3 and p53 levels. Our purpose is to approach the immunoregulation mechanism of Sirt1 in psoriasis, and provide the new target for treating psoriasis.