系统性红斑狼疮患者树突状细胞CD11c^＋，CD123^＋亚群与疾病活动性的关系

Expression and Significance of CD11c^＋ ,CD123^＋ Dendritic Ceils in Peripheral Blood of Patients with Systemic Lupus Erythematosus

目的探讨系统性红斑狼疮（systemic lupus erythematosus，SLE）患者外周血树突状细胞CD11c^＋，CD123^＋亚群与疾病活动性、肾脏损伤及血清抗ds—DNA抗体产生的关系。方法选定SLE疾病组51例、疾病对照组30例（类风湿关节炎、舍格伦综合征患者各15例）和正常对照组30例，采用流式细胞术检测上述指标。结果①SLE患者外周血树突状细胞CD11c^＋，CD123^＋亚群比例均显著低于正常对照组（P〈0．01），而疾病对照组与正常对照组之间差异无统计学意义（P〉0．05）。②疾病活动期SLE患者外周血树突状细胞CD123^＋亚群比例显著高于稳定期患者（P〈0．01），而两者CD11c^＋亚群比例之间差异无统计学意义（P〉0．05）。③SLE肾病组外周血树突状细胞CD123^＋亚群比例显著高于非肾病组患者（P〈0．01），两者CD11c^＋亚群比例之间差异无统计学意义（P〉0．05）；ds—DNA^＋组SLE患者外周血树突状细胞CD11c^＋，CD123^＋亚群比例均显著低于ds—DNA^-组（P〈0．05）。结论树突状细胞CD11c^＋，CD123^＋亚群的变化可能是SLE发病机制中的关键环节之一。

Objective To investigate the ratio of peripheral blood CD11c^＋ ,CD123^＋ dendritic ceils and explore the association with systemic lupus erythematosus（SLE） activity,nephropathy and serum anti-ds-DNA antibody. Metheds The percentage of CD11c^＋,CD123^＋ dendritic ceils in peripheral blood from 51 systemic lupus erythematosus （SLE）patients, 30 rheumatism controls（15 cases of RA and 15 cases of SS） and 30 normal individuals was measured by flowcytometer. Results ①SLE patients had statisitically lower level of CD11c^＋ ,CD123^＋ dendritic cells in peripheral blood than normal con- trols （P〈0. 01）,but no significance was found between rheumatism controls and normal controls.②Further study found that the percentage of peripheral blood CD123^＋ ceils in patients with active disease was significantly higher than patients with inactive disease （P〈0. 01）,but no significant difference was found in CD11c^＋ cells between patients with and without disease activity. ③SLE patients with nephropathy still had significantly higher levels of CD123^＋ cells than patients without nephropathy（P〈0. 01） ,but no significance was found in CD11c^＋ cells. Patients with ds-DNA had statisitically lower level of CD11c^＋, CD123^＋ dendritic cells in peripheral blood than patients without ds-DNA （P 〈 0. 05）. Conclusion The CD11c^＋ ,CD123^＋ dendritic cells may play a crucial role in the pathogenesis of SLE.