中文摘要：

目的：研究转录调节因子RUNX1及其靶基因SLC9A3R1在银屑病患者骨髓CD34^＋细胞中的表达及SLC9A3R1与NAT9之间RUNX1的连接位点,以揭示银屑病患者造血干细胞的活性,为深入阐明银屑病患者免疫异常的根源及造血细胞在其中的作用提供理论依据。方法：采用免疫磁珠法分离CD34^＋细胞,RT-PCR法分别检测RUNX1和SLC9A3R1的mRNA表达,直接测序法检测PCR产物中SLC9A3R1与NAT9之间RUNX1连接位点DNA序列。结果：银屑病患者骨髓CD34^＋细胞RUNX1表达阳性率低于正常对照组（P〈0.05）;银屑病患者骨髓CD34^＋细胞SLC9A3R1表达水平明显高于正常对照组（P〈0.05）,且与PASI评分正相关（r=0.48,P〈0.05）;在SLC9A3R1与NAT9之间未发现RUNX1连接位点的突变。结论：决定银屑病患者骨髓CD34^＋细胞分化的关键基因RUNX1存在异常;银屑病患者骨髓RUNX1和SLC9A3R1可能通过对骨髓造血微环镜和造血干细胞的异常调节参与银屑病的发病。

英文摘要：

Objective： To reveal the relation between RUNX1 and hematopoietic cells by examination of the expression of RUNX1 and its target gene SLC9A3R1 in bone marrow CD34 ^＋ cells from patients with psoriasis,as well as the RUNX1 linkage locus between SLC9A3R1 and NAT9. Methods：Bone marrow CD34 ^＋ cells were isolated from psoriatic patients and nortnal persons by immtmomagnetic cell selection. Expression of mRNA for RUNX1 and SLC9A3R1 were analyzed using reverse transcriptase-polymemse chain reaction （RT-PCR）, the RUNX1 linkage locus between SLC9A3R1 and NAT9 was detected. Results： The positive frequency of RUNX1 in bone manrrow CD34^＋ cells from patients with psoriasis was lower than in normal controls（ P 〈 0.05）.The expression of SLC9A3R1 mRNA in bone marrow CD34^＋ cells from patients with psoriasis was significantly higher than that of normal controls（ P 〈 0.05）, and positively correlate with PASI（ r = 0.48, P 〈 0.05）. We hadn＇ t found out any mutation in the RUNXI hnkage locus between SLC9A3R1 and NAT9. Conclusion： The genes are abnormal, which influences the differentiation of bone marrow CD34^＋ cells in patients with psoriasis.The abnormahty of RUNX1 and SLC9A3R1 in bone marrow of psoriasis perhaps plays a role in the pathogenesis of psoriasis.