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  • 李伟,王佳怡,肖春媛,等.IL-4通过促进CD30分子表达抑制类风湿关节炎患者T细胞功能的研究[J].同济大学学报(医学版),2021,42(4):528-533.    [点击复制]
  • LI Wei,WANG Jia-yi,XIAO Chun-yuan,et al.IL-4 inhibits T cell function in patients with rheumatoid arthritis through promoting CD30 expression[J].同济大学学报(医学版),2021,42(4):528-533.   [点击复制]
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IL-4通过促进CD30分子表达抑制类风湿关节炎患者T细胞功能的研究
李伟,王佳怡,肖春媛,陆天琳,黄新芳,韩捷
0
(同济大学附属东方医院风湿免疫科,上海200120)
摘要:
目的观察IL-4和CD30在类风湿关节炎(rheumatoid arthritis, RA)中的潜在关联,并探讨其对T细胞促炎细胞因子分泌的影响。方法选取46例活动期RA患者(RA组)及41例健康人(对照组)为研究对象,其中RA患者DAS28评分3.89~7.41分,平均(4.23±1.42)分。ELISA法测定RA血清中IL-4和sCD30含量并分析二者相关性;流式细胞术分析重组人TIL-4蛋白对PBMC来源的T细胞表面CD30表达的影响,观察IL-4刺激后CD30+T及CD30-细胞内IFN-γ、IL-17的水平变化。结果与健康对照组相比,RA患者血清中sCD30水平显著升高(P<0.0001),IL-4水平也有升高(P<0.01),Pearson相关性分析显示二者存在正相关。在抗CD3、抗CD28活化培养条件下,重组IL-4蛋白可促进RA患者外周血中T细胞表达CD30分子增加,增加程度与IL-4浓度呈正比。细胞内荧光染色显示,RA患者CD30+T细胞内IL-17较对照组明显升高(P<0.05)。重组IL-4蛋白能降低RA及对照组外周血中CD30+T细胞分泌IFN-γ、IL-17,而对CD30-T细胞内细胞因子的分泌无明显影响。结论IL-4可能通过促进T细胞上CD30分子表达降低促炎细胞因子产生,在RA中发挥免疫调节作用。
关键词:  白细胞介素-4  CD30分子  类风湿关节炎  T细胞
DOI:10.12289/j.issn.1008-0392.20481
投稿时间:2020-11-09
基金项目:上海市浦东新区科委创新基金(PKJ2016-Y61);同济大学中央高校基本科研项目(22120180467)
IL-4 inhibits T cell function in patients with rheumatoid arthritis through promoting CD30 expression
LI Wei,WANG Jia-yi,XIAO Chun-yuan,LU Tian-lin,HUANG Xin-fang,HAN Jie
(Dept. of Rheumatology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai 200120, China)
Abstract:
Objective To investigate the potential association of IL-4 and CD30 in rheumatoid arthritis and to explore their effects on T cell pro-inflammatory cytokine secretion. MethodsForty-six active RA patients with an average DAS28 score of 4.23±1.42(3.89-7.41) (RA group) and forty-one healthy subjects(control group) were enrolled in the study. The serum levels of IL-4 and sCD30 were measured by ELISA, the expression of CD30 on T cells derived from PBMC was analyzed by flow cytometry, the levels of IFN-γ and IL-17 in CD30+ T cells and CD30- T cells were determined after IL-4 stimulation. ResultsCompared with the control group, the serum sCD30 and IL-4 levels in RA patients were significantly increased (P<0.0001 and P<0.01). Pearson correlation analysis showed that there was a positive correlation between them. Under the stimulation of anti-CD3 and anti-CD28, recombinant human IL-4 protein significantly increased the expression of CD30 on T cells of RA patients in a dose-dependent manner(P<0.05). Intracellular fluorescence staining showed that IL-17 in CD30+ T cells of RA patients was significantly higher than that in healthy controls(P<0.05). IL-4 decreased the secretion of IFN-γ and IL-17 by CD30+ T cells in RA and control group but had no effect on CD30-T cells. ConclusionIL-4 may play an immunomodulatory role in RA by promoting the expression of CD30 on T cells and decreasing the production of pro-inflammatory cytokines.
Key words:  interleukin-4  CD30 molecule  rheumatoid arthritis  T cell

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