T细胞表达Fas用于评价系统性红斑狼疮活动性和疗效的价值

目的：流式细胞术检测系统性红斑狼疮(SLE)患者T细胞表面Fas表达水平，探讨其用于评价疾病活动指数和疗效的价值。方法:对36例活动期SLE患者和18名正常人群，通过流式细胞仪检测T细胞Fas表达和凋 亡率。对SLE患者分别给予泼尼松、甲泼尼龙、环磷酰胺冲击治疗，在入院3 d内、出院时（平均住院天数为22.6 d）、出院后4周分别检测T细胞Fas表达（Fas+T）。结果:活动期SLE患者T细胞表面Fas表达与T细胞凋亡率和SLEDAI之间，具有明显正相关P<0.01），皮质类固醇或免疫抑制剂治疗活动期SLE患者后，出院时T细胞表面Fas 表达（Fas+T）明显升高；出院后4周复诊时呈下降趋势。结论:SLE 患者T细胞表面Fas表达上调,由Fas介导的T细胞凋亡增强,刺激机体产生抗dsDNA等多种自身 抗体,可能是SLE免疫功能紊乱的主要原因。T细胞表面Fas密度可能是评价SLE疾病活动性和 临床疗效的主要参数。

Determination of Fas molecules on T cells and its relation with the reactiveness of SLE and therapeutic effect

AIM: To determine the expression level of Fas molecules on the T cells isolated from systemic lupus erythematosus (SLE) patients. METHODS: The expression of Fas on T cells and the apoptotic rate of 36 patients with SLE in active phase and 18 normal people were determined with flow cytometry. The patients were treated with impact therapy of prednisone, methylprednisolone or cyclophosphamide, respectively, according to their conditions. Within 3 days after admission, immediately before discharging (the average days in hospital is 22.6 d), and 4 weeks after discharging, the amount of Fas molecules expressed on T cell surface was determined respectively with flow cytometry in each patient. RESULTS: There was a positive correlation between SLEDAI, apoptotic rate of T cells and Fas molecules on T cells in SLE patients of active phase (P<0.01). After corticosteroid or immunosuppressant treatment in active phase of SLE patients, when discharging from hospital, the amount of Fas molecules on T cell significantly increased (Fas~ T), and 4 weeks after discharging, the Fas molecules on T cells were decreased. CONCLUSIONS: The amount of Fas molecules expressed on T cell from SLE patients increases. The Fas-mediated apoptosis in T cells stimulates the body to generate many kinds of autoantibody, such as anti-dsDNA, which perhaps is the main cause that leads to the immune dysfunction of SLE. The density of Fas molecules on T cell surface may be a main parameter in evaluating the reactiveness of SLE and clinic therapeutic effect.