前期研究我们在国际上首先发现银屑病造血干细胞（HSC）分化的T细胞与银屑病T细胞具有许多相似的免疫特性，且Notch信号转导多个环节障碍参与了银屑病HSC向T细胞分化。Notch信号可调节RUNX1表达，而RUNX1是调节HSC和T细胞分化的主控基因，新近我们又得到银屑病HSC RUNX1部分靶基因异常的直接证据。故对RUNX1的深入研究将使银屑病HSC向T细胞分化机理变的更加清楚。本课题拟在前期基础上对银屑病CD34+细胞进行以下研究：①检测 SCL表达、DNA甲基化和组蛋白乙酰化；②转染PRMT1/干扰RUNX1表达，检测转染/干扰对RUNX1蛋白甲基化、与SLC9A3R1蛋白-DNA相互作用、SLC9A3R1表达及细胞粘附的影响；③将转染/干扰后CD34+细胞定向分化为T细胞，检测其对T细胞分化和靶基因表达的影响；④分选外周血T细胞，检测RUNX1靶基因表达等。课题是实质性原创项目。

We had found that many immuno-character of T cell differentiated from psoriatic hematopoietic stem cell(HSC) were similar to T cell from psoriatic peripheral blood in previous study, and most of the abnormality in Notch signal particpate in the psoriatic differentiation of HSC to T cell. The expression of RUNX1 which play critical role in HSC and differentiation of T cell, was regulated by Notch signal.Recently,our studies indicated that target genes of RUNX1 were abnormal in HSC from psoriasis.The further study of RUNX1 will make the differentiated mechasim of HSC to T cell become clearer in psoriasis.In this study,expression of SCL,methylation of DNA and acetylation of histone will be tested in CD34+ cell. Secondly,the expression or protein methylation of RUNX1 will be interfered.After that the impaction will be invested including protein methylation of RUNX1,interaction between RUNX1 protein and SLC9A3R1, expression of SLC9A3R1 and function of cell adhesion. CD34+ cell will also be differentiated to T cell after interfere, then activity of T cell and expression of RUNX1 target genes be invested. At the same time, the T cell separated from psoriatic peripheral blood will also be tested.The topic is original.