系统性红斑狼疮患者外周血CD3^＋ CD56^＋自然杀伤样T细胞体外活化特性研究

The study of biological features of CD3^+ CD56^+ NKT like cells in peripheral blood of patients with systemic lupus erythematosus

目的探讨系统性红斑狼疮(SLE)患者外周血CD3+CD56+自然杀伤样T(NKT样)细胞的表达以及体外活化后的增殖能力和生物学特性。方法采用流式细胞仪检测30例SLE患者(疾病活动组20例,稳定组10例)和20例正常对照组外周血CD3+CD56+NKT样细胞的表达及不同体外刺激活化后的增殖能力。通过检测Th1型细胞因子干扰素γ(IFN-γ)和Th2型细胞因子白介素(IL)-4表达水平来判断其在调节炎症免疫反应中的作用。结果 SLE患者外周血CD3+CD56+NKT样细胞的表达明显低于正常对照组,差异有统计学意义(P<0.05),而SLE疾病活动组与稳定组之间差异无统计学意义。与佛波酯(PMA)和离子霉素的非特异性刺激相比,经抗CD3单克隆抗体和IL-2特异性诱导刺激对CD3+CD56+NKT样细胞的增殖能力更强,Th1型细胞因子IFN-γ表达水平更高,差异有统计学意义(P<0.05),而Th2型细胞因子IL-4在两种刺激条件下几乎均不表达。结论 CD3+CD56+NKT样细胞通过分泌Th1型细胞因子IFN-γ来调节炎症免疫作用,SLE的发病可能与外周血CD3+CD56+NKT样细胞表达数量减少及其免疫功能严重失调有关。

Objective To investigate the level and biological features of CD3＋CD56＋ NKT like cells in peripheral blood of patients with systemic lupus erythematosus（SLE）.Methods The expression level and proliferation capacity of CD3＋CD56＋ NKT like cells by different stimulating methods in vitro flow cytometry were detected by in 30 patiens of SLE（20 cases of active patients and 10 cases of stable patients） and 20 healthy controls.The effect of CD3＋CD56＋ NKT like cells in the regulation of inflammatory immune response were distinguished by detecting IFN-γ of Th1 cytokines and IL-4 of Th2 cytokines.Results The expression level of CD3＋CD56＋ NKT like cells in SLE patients decreased significantly than that in healthy controls（P 0.05）.However,the expression level of CD3＋CD56＋ NKT like cells in active group was no statistical significance with stable patients.Compared with the proliferation capacity of CD3＋CD56＋ NKT like cells by the activation of anti-CD3mAb and IL-2 enhanced significantly compared with by nonspecific stimulation of PMA and Ionomycin.The expression level of IFN-γ of Th1 cytokines was increased markedly by the activation of anti-CD3mAb and IL-2（P 0.05）.However,the level of IL-4 of Th2 cytokines was scarcely expressed by two different stimulating methods.Conclusion CD3＋CD56＋ NKT like cells regulate the inflammatory immune response by IFN-γ of Th1 cytokines,and the pathogenesis of SLE may be related to the decline in the number of NKT like cells and their serious imbalance of immunologic function.