肿瘤坏死因子样配体1A对类风湿关节炎患者外周血Th17产生及分化的调节作用  

Role of tumor necrosis factor like ligand-1A aberrance in the generation and differentiation of peri- pheral blood Th17 in rheumatoid arthritis

作　　者：周敏[1] 刘蕊[1] 李霞[3] 孙凌云[2] 

机构地区：[1]南京医科大学鼓楼临床医学院,210008 [2]南京大学医学院附属鼓楼医院风湿免疫科 [3]大连医科大学基础医学院免疫教研室

出　　处：《中华风湿病学杂志》2013年第8期518-521,共4页Chinese Journal of Rheumatology

基　　金：国家自然科学基金（81172847）;中国博士后科学基金（2012M510073）;

摘　　要：目的探讨肿瘤坏死因子样配体1A（TL1A）对类风湿关节炎（RA）患者外周血n17产生及分化的影响。方法分离RA患者外周血单个核细胞（PBMCs），加植物血凝素（PHA）和TL1A刺激，或磁珠分选RA患者外周血初始T细胞，在诱导其向n17分化同时加入TL1A，流式细胞术（FCM）检测Th17百分率；RA患者和健康对照组PBMCs中CD4＋ DR3＋T细胞比例亦用FCM检测。采用t检验及U检验进行统计学分析。结果TL1A可上调RA患者外周血Th17比例[（7．5±2．3）％与（5．2±1．5）％，t=2．647，P〈0．05]，并可显著诱导初始T细胞向n17分化[（37．7±1．9）％与（29．5±2．0）％，t=6．455，P〈0．05]；RA患者外周血CD4＋ DR3＋T细胞百分率[（0．56±0．87）％]明显高于健康对照组[（0．13±0．04）％，P〈0．05]；PHA刺激可明显增加RA患者外周血CD4＋DR3＋T细胞比例[（4．51±1．36）％与（1．11±0．29）％，t=2．915，P〈0．05]，但对健康对照组CD4＋DR3＋T细胞比例无影响[（0．199±0．104）％与（0．072±0．029）％，t=1．644，P=-0．1988]。结论TL1A可促进RA患者外周血Th17产生和分化；TL1A可能是通过与DR3结合介导这一作用。Objective To investigate the role of TLIA in the generation and differentiation of peripheral blood Thl7 in rheumatoid arthritis. Methods The peripheral blood mononuelear cells （PBMCs） of RA were isolated and stimulated with PHA in the presence or absence of TL1A. Naive CD4＋ T cells from RA was cultured under Thl7-polarizing conditions with or without TL1A. The percentage of Thl7 was detected by flow cytometry （FCM） analysis. The DR3 expression on CD4＋ T cells from PBMCs of RA patients and healthy controls （HC） were analyzed by using FCM. Data were analyzed with t test and U test. Results TL1A could significantly up-regulate the percentage of Thl7 in PBMCs of RA [ （7.5±2.3）% vs （5.2±1.5）%, t=2.647, P〈 0.05]. Compared to the HC groups, TLIA could significantly induce Th17 differentiation from naive T cells [（37.7±1.9）% vs （29.5±2.0）%, t=6.455, P〈0.05]. The percentage of CD4＋DR3＋ T cell in PBMCs of RA [（0.56±0.87）%] was significantly higher than that of HC [（0.1±0.04）%） P〈0.05]. The percentage of CD4＋ DR3＋ T cell in PBMCs when stimulated with PHA was increased in RA patients, [（4.51±1.34）% vs （1.11± 0.29）%, t=2.915, P〈0.05], but no obvious increase in HC [（0.199±0.104）% vs 0.072%±0.029）%, t= 1.644, P=0.1988]. Conclusion TL1A can promote the generation and differentiation of Th17 in the PBMCs of RA, and this effect may be mediated by the binding of TL1A with DR3.

关 键 词：关节炎 类风湿 肿瘤坏死因子样配体-1A TH17 死亡受体3 

分 类 号：R593.22[医药卫生—内科学]