羟氯喹抑制紫外线诱导的系统性红斑狼疮CD4^＋T细胞白细胞介素-10和干扰素-γ的表达  

Hydroxychloroquine inhibits ultraviolet-induced expression of interleukin-lO and interferon-γ fromCD4^＋T cells in patients with systemic lupus erythematosus

作　　者：陈学琴[1] 汪国生[1] 张敏[1] 赵小娟[1] 张宏[1] 李向培[1] 

机构地区：[1]安徽医科大学附属省立医院风湿免疫科,合肥230001

出　　处：《中华风湿病学杂志》2011年第6期365-368,共4页Chinese Journal of Rheumatology

基　　金：国家自然科学基金（81072462）;安徽省自然科学基金（090413253）;安徽省高校省级自然科学研究项目（KJ2010A188）

摘　　要：目的研究紫外线对系统性红斑狼疮（SLE）CD4^＋T细胞因子的影响和羟氯喹的抑制作用。方法选择SLE30例，健康对照10名。磁珠分选SLE患者和健康人的CD4＋T细胞，紫外线311nm窄谱中波紫外线暴露，加入羟氯喹共培养，酶联免疫吸附试验（ELISA）检测培养上清白细胞介素（IL）-10和干扰素一1的表达水平。采用t检验进行统计学分析。结果SLE患者CD4^＋T细胞IL-10表达高于健康对照[（27±4）和（18±3）pg／ml，P=O．011]；经45、100mJ／cm。紫外线暴露后，SLE活动患者CD4＋T细胞IL-10表达升高[（27±4）和（77±42）pg／ml，（40±18）和（77±42）pg／ml，P=O．022，P=O．048]，经100mJ／era。紫外线暴露后，活动患者CD4＋T细胞IL一10表达高于稳定患者[（77＋42）和（24±4）pg／ml，P=O．029]；羟氯喹降低SLE活动患者CD4＋T细胞IL一10和干扰素一叫表达[（2．6＋4．0）和（17．9±2.3）pg／ml，P=O．018，P=-0．017）]；羟氯喹降低经45，100rnJ／cm2紫外线暴露后SLE活动患者T细胞IL一10表达[（40±18）和（22±6）pg／ml，（77±42）和（2l±5）Dg／ml，P=O．037，P=0．04]；羟氯喹降低经100mJ／cm^2紫外线暴露的SLE活动和稳定患者T细胞干扰素一1表达[（18＋3）和（13±14）pg／ml，（19±7）和（12±5）pg／ml，P=0．013，P=0．049]。结论紫外线加重SLE患者体内Thlfrh2细胞因子的比例失衡；羟氯喹抑制了紫外线诱发SLE患者干扰素-γ和IL-10的表达。Objective To explore the role of hydroxychloroquine （HCQ） in uhraviolet B （UVB）- induced expression of interleukin （IL）-10 and interferon （IFN）-γ from CD4^＋T ceils in patients with systemic lupus erythematosus （SLE）. Methods Thirty patients with SLE and 10 healthy controls were enrolled in the study. CD4^＋T cells were isolated using magnetic beads from SLE patients and healthy controls. HCQ was added in culture media before and after irradiation with UVB 311 nm narrow band ultraviolet B （NB-UVB）. The levels of IL-10 and IFN-γ in the supernatant were detected with enzyme-linked immunosorbent （ELISA）. Comparisons between groups were performed by t-test. Results The level of IL-10 was higher in SLE patients [ （27±4） pg/ml ] than that in healthy controls [ （ 18±3 ） pg/ml, P=0.011 ]. After exposure of CD4^＋T cells to UVB in 45 or 100 m,l/cm2 dosages, the level of IL-10 was increased significantly in patients with active disease （P=0.022, P=0.048）. After exposure of CD4^＋T cells to UVB in 100 mJ/cm2 dosages, the levels of IL-10 was higher in patients with active disease [ （77±42） pg/ml] than patients with stable disease [ （24± 4） pg/ml, P=0.029]. When CD4^＋T cell were cultured with HCQ, IL-10 and IFN-γ levels in patients with active disease [（2.6±4.0）, （17.5±2.3） pg/ml] were decreased significantly （P=0.O18, P=0.017）. HCQreversed UVB-induced IL-10 expression in active SLE patients after exposure of CDd^T cel｜s to UVB in 45 or 100 mJ/cm^2 dosages （P=0.037, P=0.04）. HCQ also reversed UVB-induced IFN-γ expression in active SLE patients and stable SLE patients after exposure to CD4^＋T ceils with UVB in 100 mJ/cm^2 dosages （P=0.013, P= 0.049）. Conclusion UVB can aggravate the imbalance of Thl and Th2 cytokines. HCQ inhibits UVB- induced IL-10 and IFN-γexpression of CD4^＋T ceils in patients with SLE, especially in patients with active disease.

关 键 词：红斑狼疮 系统性 紫外线 羟氯喹 CD4^+T细胞 

分 类 号：R593.241[医药卫生—内科学]