急性冠状动脉综合征患者外周血辅助性T细胞和调节性T细胞的检测意义

Role of detecting Th17/Treg in acute coronary syndrome patients

目的探讨外周血辅助性T细胞(Th17)和调节性T细胞(Treg)平衡在急性冠状动脉综合征(ACS)患者中的变化和意义。方法选择79例冠心病患者分为急性心肌梗死(AMI)组22例、不稳定性心绞痛(UAP)组19例、稳定性心绞痛(SAP)组18例及胸痛综合征(CPS)组20例,用流式细胞术检测外周血中Th17(其占CD3T淋巴细胞比例)及Treg(其占CD4T淋巴细胞比例)的表达,ELISA检测血清Th17及Treg的相关细胞因子白细胞介素(IL)-17和IL-10水平。结果与CPS组和SAP组比较,UAP组及AMI组Th17表达[(2.97±0.62)%和(3.58±1.02)%vs(0.59±0.27)%和(1.37±0.44)%]及血清中IL-17水平显著升高[(41.92±8.89)ng/L和(52.27±9.49)ng/L vs(10.32±2.05)ng/L和(14.73±4.74)ng/L,P<0.01],Treg表达及血清中IL-10水平显著降低(P<0.01)。SAP组Th17表达及IL-17水平也显著高于CPS组,Treg表达及IL-10水平显著低于CPS组(P<0.05,P<0.01)。与CPS组和SAP组比较,UAP组和AMI组Th17/Treg比值显著升高(P<0.01),SAP组Th17/Treg比值显著高于CPS组(P<0.01)。结论 ACS患者外周血中Th17/Treg失衡可能促进了冠状动脉粥样硬化斑块不稳定的进展并进一步诱导ACS的发病。

Objective To study the role of Th17/Treg balance in acute coronary syndrome（ACS）patients.Methods Seventy-nine coronary heart disease patients were divided into acute myocardial infarction（AMI）group（n=22）,unstable angina pectoris（UAP）group（n=19）,stable angina pectoris（SAP）group（n=18）,and chest pain syndrome（CPS）group（n=20）.Expressions of Th17 and Treg in peripheral blood were detected by flow cytometry and serum levels of IL-17 and IL-10 in Th17and Treg were measured by ELISA.Relationship of Th17 and Treg with the occurrence and progression of ACS was studied.Results The proportion of circulating Th17 in CD3＋T and the serum IL-17 level were significantly higher whereas the proportion of circulating Treg in CD4＋T and the srum IL-10 level were significantly lower in UAP group and AMI group than in CPS group and SAP group（P〈0.01）.The proportion of circulating Th17 and the serum IL-17 level were significantly higher whereas the proportion of Treg and the serum IL-10 level were significantly lower in SAP group than in CPS group（P〈0.05,P〈0.01）.The ratio of Th17/Treg was significantly higher in UAP group and AMI group than in CPS group and SAP group and in SAP group than in CPS group（P〈0.01）.Conclusion The imbalanced Th17/Treg can promote the formation of unstable coronary atherosclerotic plaques and induce ACS.