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作 者:许荣 赵蓉[2] 钱柳[2] 胡朝英[3] 苗平[2] 余奇文[2] 李云春 何东仪 张冬青[2]
机构地区:[1]上海市长宁区光华中西医结合医院中心实验室,200052 [2]上海市免疫学研究所 [3]上海市徐汇区中心医院中心实验室
出 处:《中华风湿病学杂志》2014年第5期297-301,共5页Chinese Journal of Rheumatology
基 金:国家自然科学基金(31270963);上海市科委自然科学基金(11ZR1427000);上海市科委重点项目(1OJC1408500,10ZR1426100);上海市徐汇区中心医院院基金(2011XHCH07)
摘 要:目的分析RA患者外周血和关节滑膜液中γδT细胞亚群及其与RA发病的关联性。方法采用流式细胞仪检测健康人外周血、RA患者外周血PBMCs及滑膜液单个核细胞(SFMCs)中Vγ9Vδ2T细胞亚群;ELISA法检测在OA患者滑膜液、RA患者血清和滑膜液、RA患者PBMCs和SFMCs培养上清中IFN-γ/和IL-17的表达水平;氚-胸腺嘧啶核苷(3H—TdR)掺入法检测PBMCs和SFMCs对抗原肽的应答能力,以及18T细胞的抗原递呈能力。采用t检验、单因素方差分析进行统计学分析。结果RA患者外周血中效应记忆型Vγ9Vδ2T细胞占叫8T细胞的(48.2±17.6)%,并有(42.8±17.7)%和(2.2±1.5)%的v19v82T细胞表面分别表达HLA—DR4和CD86分子;关节滑液中效应记忆型Vγ9Vδ2T细胞占18T细胞的(62.9±7.9)%,并有(85.8±1.7)%和(17.3±2.0)%的Vγ9Vδ2T细胞表面分别表达HIJA—DR4和CD86分子。RA患者的PBMCs和SFMCs具有分泌IFN-γ和IL-17炎症因子的特征,且较健康人PBMCs相比,对抗原肽具有更强的免疫反应。同时实验结果还表明RA患者的叮γδT细胞的抗原递呈能力较B细胞强。结论γδT细胞在RA的发病过程中不仅通过分泌细胞因子与炎症细胞协同作用参与炎症反应,而且通过特异性免疫应答的机制发挥树突状细胞样的作用,不断将病毒肽和自身抗原肽递呈给CD4+T细胞。Objective To analyze subsets of γδT T cells in rheumatoid arthritis (RA) patients' periph- eral blood and synovial fluid and its correlation with the pathogenesis of RA. Methods Flow cytometry was used to analyze the Vγ9Vδ2T T cell subsets in human peripheral blood, peripheral blood mononuclear cells (PBMCs) and synovial fluid mononuclear cells (SFMCs) of RA patients. ELISA was used to detect IFN-'y and IL-17 in the synovial fluid of osteoarthritis (OA) patients', the serum of RA patients, synovial fluid and the cell cuhure supernatant of RA patients' PBMCs and SFMCs; 3H-TdR was labeled to detect the proliferation of PBMCs and SFMCs induced by antigen peptides, and the antigen-presenting of γδ T cell. Data were analyzed using t-test and One-way ANOVA analysis. Results The research showed that in γδ T cells of RA patients' peripheral blood, (48.2±17.6)% were effector memory Vγ9Vδ2T T cells, (42.8±17.7)% and (2.2±1.5)% Vγ9Vδ2T T cell expressed HLA-DR4 and CD86. While in RA patients' synovial fluid, (62.9±7.9)% were effector memory-type Vγ9Vδ2T T ceils, (85.8±1.7)% and (17.3±2.0)% Vγ9Vδ2T T cell expressed HLA-DR4 and CD86. The PBMCs and SFMCs of RA patients could seerete IFN-γand IL-17, and their antigen peptide immunogenieity was stronger than that of healthy human PBMCs. The results also showed that the antigen- presenting ability of γδ T eells was stronger than B cells. Conelusion The results suggest that γδ T eells participat in the pathogenesis of RA, not only by interacting with inflammatory eells to aggravate autoimmune disorder, but also contributing to specific immune response by acting as DCs-like eells-presenting antigen toCD4+ T cells persistently.
关 键 词:关节炎 类风湿 抗原呈递 ΓΔT细胞 效应记忆型Vγ9Vδ2T细胞
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