| 引用本文： |
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陈海燕,韩捷,周洁如,等.类风湿关节炎外周血和关节液树突状细胞的膜分子表达及功能研究[J].同济大学学报（医学版）,2010,31(4):70-74. [点击复制]
- CHEN Hai-yan,HAN Jie,ZHOU Jie-ru,et al.Expression of membrane molecules and function of DC in PBMC and SFMC from patients with rheumatoid arthritis[J].同济大学学报（医学版）,2010,31(4):70-74. [点击复制]
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| 摘要: |
| 目的研究类风湿关节炎（rheumatoid arthritis，RA）患者树突状细胞（dendritic cell，DC）的膜分子表达水平和功能的变化，探讨DC在RA发病机制中的作用。方法应用流式细胞术、混合淋巴细胞培养测定诱导DC细胞表面分子表达、对同种异体T细胞功能情况，诱导成熟后DC表面分子表达与临床活动及预后相关指标ESR、CRP、RF、Stoke指数的相关性。结果RA外周血来源DC表达CD83、CD209、CD80、HLA—DR较正常人外周血来源DC增高（P〈0．05），RA关节液来源DC较RA外周血来源DC表达CD83、CD209、CD86、CD80明显增高（P〈0．05）。RA关节液组较RA和正常人外周血DC对同种异体T细胞的刺激明显增强。RA患者外周血诱导成熟DC表型CD83、CD209与stoke评分指数呈正相关。结论提示RA时关节内免疫反应可能与局部DC分化、成熟能力增强有关，后者可通过激活T细胞引起自身免疫反应，造成滑膜组织损伤。RA患者DC表面共刺激分子表达水平的增高可能与患者免疫亢进及所致的免疫损伤有关。 |
| 关键词: 类风湿关节炎 树突状细胞 共刺激分子 |
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| Expression of membrane molecules and function of DC in PBMC and SFMC from patients with rheumatoid arthritis |
| CHEN Hai-yan,HAN Jie,ZHOU Jie-ru,FAN Lu |
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| Abstract: |
| Objective To investigate expression of membrane molecules and function of dendritic cell （DC） in PBMC and SFMC from RA patients and to analysis its pathogenesis role in RA development. Methods Using flow cytometry to measure the expression levels of membrane molecules. The allogeneic T cell function was detected by using mixed lymphocyte culture technique. The expression levels of membrane molecules from induced mature DC were analyzed with clinical data. Results The expression levels of CI~3, CD209, C DS0, HLA-DR on DC in PBMC from RA were significantly higher than that in control group （P 〈 0. 05）, CD83, CD209, CDR）, HLA-DR expression levels on DC from RA SFMC were the highest in all groups. Allogeneic T cell function from RA SFMC group was significantly higher than that from control group and RA PBMC group. More interestingly, elevated expression of CD83, CD209 from induced mature DC were positively correlated with Stoke score index. Conclusion Intra-articular immune response from RA may be related to enhance the capacity of local DC differentiation and maturation, which may stimulate T cell activation and cause autoimmune response, resulting in synovial tissue damage. Elevated expression levels of membrane molecules from RA patients may be related to hyperfuncfion of immunity and immune damage. |
| Key words: rheumatoid arthritis dendritic cells co-stimulatory molecules |
