银屑病的发病机制尚不完全明确，研究角质形成细胞过度增殖和异常分化相关分子机制是阐明银屑病发病机制的关键。本研究前期采用RNA-Seq技术检测分析银屑病相关长链非编码RNA（lncRNA），发现大量可能与银屑病密切相关的lncRNA，这些lncRNA部分参与表皮分化复合物的形成，部分直接影响细胞因子调控。然而，lncRNA在银屑病中是否并如何发挥作用还有待深入研究。我们前期研究筛选得到LncRNA CTB-147C22.9可能与银屑病的发生发展密切相关，干扰此lncRNA能显著抑制角质形成细胞的的增殖和迁移能力。本项目将LncRNA CTB作为研究银屑病发病机制的切入点，通过体外细胞实验，咪喹莫特和IL-23诱导银屑病小鼠模型以及相关转基因修饰动物模型并检测一定数量的病人标本，深入探索LncRNA CTB在银屑病发病中的作用机制并明确LncRNA CTB可否成为治疗银屑病的靶点。

The precise etiology of psoriasis remains obscure. The molecular basis for excessive proliferation and abnormal differentiation in keratinocytes is one of the key factors toward clarifying the pathogenesis of psoriasis. Using RNA-seq profiling analysis, study first found a large amount of long non-coding RNA (lncRNA) related to psoriasis. Some of those are involved in the formation of epidermal differentiation complex, and others have a direct influence on the regulation of cytokines. However, there exists a dearth of information regarding the detailed mechanisms of lncRNA in the pathogenesis of psoriasis. Our preliminary data suggests that lncRNA CTB-147C22.9 may be related to the development of psoriasis. Interference of this lncRNA significantly inhibited the proliferation and migration of keratinocytes. Thus, we use lncRNA CTB as the focus of the study. We plan on investigate the mechanisms of lncRNA CTB in psoriasis through in vitro and in vivo experiments, including Imiquimod and IL-23 induced psoriasis mouse model and transgenic animal models, as well as a relatively large cohort of psoriasis patient samples. Our results will also provide new insights into lncRNA CTB as potential therapeutic targets.