类风湿关节炎患者外周血中糖皮质激素诱导的肿瘤坏死因子受体相关基因及其配体的表达和意义

目的:研究糖皮质激素诱导的肿瘤坏死因子受体家族相关基因(GITR)与其配体(GITRL)在类风湿关节炎(RA)患者外周血中的表达及其与临床指标的相关性,探讨GITR/GITRL 在RA中的意义.方法:采用实时荧光定量PCR法检测RA组(n=53)、骨关节炎(OA)组(n=35)及正常对照组(n=35)外周血GITR/GITRL mRNA含量,同时利用流式细胞仪检测上述三组患者的GITR在CD4+CD25+ T细胞的表达,并研究GITR mRNA与RA患者DAS28评分、抗环瓜氨酸(CCP)抗体、C反应蛋白(CRP)、红细胞沉降率(ESR)及类风湿因子(RF)的关系.结果:RA患者外周血GITR mRNA水平和GITRL mRNA水平(分别为12.38±5.72,16.41±10.16)明显高于正常对照组(分别为8.75±3.78,11.99±8.42)及OA组(分别为9.59±5.87,12.09±7.53;均P＜0.05).RA患者与OA组及正常对照组比较,外周血CD4+CD25+GITR+T细胞的比例也明显增高[分别为(28.12±16.85)%,(21.01±14.42)%,(19.98±9.40)%,均P＜0.05].RA患者GITR mRNA表达水平与DAS28评分及ESR呈明显正相关(r值分别为0.361和0.427,P＜0.01).结论:RA患者GITR/GITRL表达增多,与RA发病及疾病活动度有关.

GITR/GITRL expression in peripheral blood of rheumatoid arthritis

OBJECTIVE:To explore the expression of GITR/GITRL in rheumatoid arthritis(RA) and its correlation with clinical features of the disease. METHODS:Fifty three RA patients, 35 osteoarthritis (OA) patients and 35 healthy volunteers were included in the study. The real-time-fluorescence quantitative PCR method was used to analyze the expression level of GITR/GITRL mRNA. Using fluorescence-activated cell sorting(FACS), the expression of GITR on CD4+CD25+ T cells in peripheral blood monouuclear cells (PBMC) was detected. The levels of Anti-CCP antibody, C-reactive protein(CRP), erythrocyte sedimentation rate(ESR) and rheumatoid factor (RF) of the RA patients were measured at the same time. RESULTS: It was shown that the level of GITR/GITRL mRNA and the percentage of GITR+ T cells in the CD4+CD25+ T cell subpopulation[12.38+/-5.72/16.41+/-10.16,(28.12+/-16.85)%] were significantly higher than those of the OA group [9.59+/-5.87/12.09+/-7.53,(21.01+/-14.42)%,P<0.05] and control group [8.75+/-3.78/11.99+/-8.42,(19.98+/- 9.40)%,P<0.05]. The expression of GITR/GITRL from RA patients was positively associated with the level of DAS28 and ESR (r=0.361,r=0.427,P<0.01). CONCLUSION: The GITR/GITRL expression of RA patients was higher than that of other groups which may play an important role in the development of RA.