CD4^+CD25^+Foxp3^+调节性T细胞在类风湿性关节炎及骨关节炎患者外周血和关节液中含量的变化

CD4^+CD25^+Foxp3^+ Regulatory T Cell Content in Peripheral Blood and Synovial Fluid of Patients with Rheumatoid Arthritis and Osteoarthritis

目的分析CD4+CD25+Foxp3+调节性T细胞(Regulatory T cell,Treg)在类风湿性关节炎(Rheumatoid arthritis,RA)及骨关节炎(Osteoarthritis,OA)患者外周血和关节液中含量的变化,探讨其在RA中可能的意义。方法以肝素抗凝负压采血管分别抽取36例RA患者、30例OA患者和33名健康人外周静脉血,常规关节穿刺术抽取RA和OA患者膝关节腔积液,采用流式细胞术分别检测CD4+CD25+Foxp3+Treg细胞的百分含量。结果 RA组外周血中CD4+CD25+Foxp3+Treg细胞的百分含量显著低于OA组和健康对照组(P<0.05),OA组与健康对照组相比,差异无统计学意义(P>0.05);RA组关节液中CD4+CD25+Foxp3+Treg细胞的百分含量显著高于OA组(P<0.01);RA组和OA组关节液中CD4+CD25+Foxp3+Treg细胞的百分含量均显著高于自身外周血(P<0.01)。结论 CD4+CD25+Foxp3+Treg细胞在RA患者中的负性调控作用降低,可能是促进疾病发生发展的一个不可缺少的因素,但在关节液中,可能更主要是表现为炎症发生后的继发性反应。

Objective To analyze the CD4＋CD25＋Foxp3＋ regulatory T cell（Treg） contents in peripheral blood and synovial fluid of patients with rheumatoid arthritis（RA） and osteoarthritis（OA） and investigate the potential role of Treg in RA.Methods The peripheral blood samples of 36 patients with RA,30 patients with OA and 33 healthy volunteers were collected using blood collection tube with negative pressure,and the synovial fluid of patients with RA and OA by routine articulus puncturation,then determined for CD4＋CD25＋Foxp3＋ Treg content.Results CD4＋CD25＋Foxp3＋ Treg content in peripheral blood of patients with RA was significantly lower than those of patients with OA and those of healthy volunteers（P 0.05）.However,the CD4＋CD25＋Foxp3＋ Treg in peripheral blood of patients with OA showed no significant difference with that of healthy volunteers（P 0.05）.The CD4＋CD25＋Foxp3＋ Treg content in synovial fluid of patients with RA was significantly higher than that with OA（P 0.01）.Both the CD4＋CD25＋Foxp3＋ Treg contents in synovial fluid of patients with RA and OA were significantly higher than those in peripheral blood of the same groups（P 0.01）.Conclusion A decreased negative regulation of CD4＋CD25＋Foxp3＋ Treg was observed in the patients with RA,which might be an indispensable factor for disease.However,it was more likely to be a secondary action after inflammation in synovial fluid.