心肌梗死后心功能不全患者辅助性T细胞功能失衡及意义

目的 探讨心肌梗死(MI)后心功能不全患外周血辅助性T淋巴(Th)细胞功能失衡及意义。方法43例MI患发病后1个月时,按照纽约心脏病协会(NYHA)心功能分级分为两组：MI1组(Ⅰ、Ⅱ级)和MI2组(Ⅲ、Ⅳ级),对两组患进行心脏超声检测心功能指标。采用流式细胞分析法,检测两组患外周血CD4^ 细胞胞内细胞因子干扰素γ(IFN-γ)和白介素4(IL-4)的表达。同时分离外周血单个核细胞(PBMC),经植物血凝素(PHA)刺激培养后,应用酶联免疫吸附方法(ELISA)检测培养液上清中IFN-γ和IL-4水平。结果MI2组患IFN-γ染色阳性的细胞占CD^ T细胞的比率(16．9％)明显高于MI1组(13．3％),IL-4染色阳性细胞比率在两组间差异未见统计学意义。ELISA检测显示MI2组培养液上清中IFN-γ水平及IFN-γ/IL-4比值明显高于MI1组,而两组间IL-4水平差异无统计学意义。结论MI后患Th细胞功能与心功能有一定关系,心功能差的患。Th1细胞功能明显亢进。Th细胞功能失衡可能参与了MI后的心室重构过程。

The significance of Th1/Th2 function imbalance in patients with post-infarction cardiac insufficiency

OBJECTIVE: To study the significance of Th1/Th2 function imbalance in patients with post-infarction cardiac insufficiency. METHODS: Forty-three MI (myocardial infarction) patients were divided into 2 groups one month after the onset according to the New York Heart Association (NYHA) classification system: group MI 1 (I, II) 25 patients and group MI 2 (III, IV) 18 patients. At the same time, the heart function was evaluated by two-dimensional echocardiography. Peripheral blood mononuclear cells (PBMCs) were collected from these patients. Cytokine-producing CD4 + T cells were quantified by 3-color flow cytometry after being stimulated with phorbol myristate acetate (PMA) and ionomycin. After being stimulated with PHA, the levels of IFN-gamma and IL-4 in culture supernarants were measured by ELISA. RESULTS: The frequencies of IFN-gamma-producing T cells were found to be significantly higher in group MI 2 (16.8%) than that in group MI 1 (13.1%). There was no significant difference on the frequencies of IL-4-producing peripheral T cells between the two groups. The IFN-gamma level and the ratios of IFN-gamma/IL-4 in group MI 2 were significantly higher than those in group MI 1, while there was no significant difference in IL-4 levels between the two groups. CONCLUSIONS: The Th-cell function was associated with heart function in post MI patients. The up-regulation of Th1 cell function was consistent with poor heart function, suggesting that Th1/Th2 cell function imbalance may participate in ventricular remodelling after MI.