免疫细胞基因表达的表观调控机制与自身免疫性疾病的关系受到高度关注。SLE是严重危害人类健康的自身免疫病，发病机制复杂，但基因表达调控导致的免疫细胞功能异常是关键。长链非编码RNA(lncRNA)作为细胞内大量存在的重要非编码RNA，其调控免疫细胞的作用和SLE的关系受到人们重视成为新的研究热点。我们采用lncRNA芯片筛选出SLE患者外周血T细胞中差异表达的CUST52998等多个，在此基础上本课题拟进一步研究lncRNA 调控T细胞的功能和相关机制。采用生物信息学分析、荧光素酶共转染及RNA pulldown技术确定与CUST52998直接作用的分子。构建慢病毒高表达或干扰表达T细胞中CUST52998，探讨lncRNA对T细胞表型、性状和功能发挥的调节作用和机制，为进一步认识lncRNA对T细胞功能的表观调控机制以及lncRNA在SLE发生发展中的作用、更有效地防治SLE提供实验依据。

The relationship between epigenetic regulation on gene expression of immune cells and autoimmune disease have been highly concerned by researchers. Systemic lupus erythermatosus (SLE) is a fatal autoimmune disease with complex etiology. Although the pathogenesis of SLE is still unclear, abnormal activity of immune cells caused by disregulation of gene expression play a key role in the development of SLE. Long non-coding RNAs(lncRNAs), an important fraction of the untranslated RNA molecules, participate in diverse important biological processes through distinct mechanisms. The roles of lncRNA on immune cells regulation in the pathogenesis of SLE have attracted much attentions.In this study, we applied lncRNA microarray to elucidate the lncRNA expression profile of T cells in SLE, and found that several lncRNA expressions such as CUST52998 were markedly elevated in SLE patients.We intend to further explore the role of lncRNA on T cell regulation.We use bioinformatic，luciferase reporter gene and RNA pull down techniques to conform the target genes of lncRNA CUST52998, and further construct lentiviral vector overexpressing or inhibiting lncRNA CUST52998 to analyze the detailed mechanisms of CUST52998 on T cell function. This reasearch will be helpful for us to further clarify the epigenetic regulation mechanisms of T cell abnormality in SLE development and provide experimental clues for the disease prevention and treatment.