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Phenotypic and Functional Alterations on Inflammatory Peripheral Blood Cells After Acute Myocardial Infarction

机译:急性心肌梗死后炎性外周血细胞的表型和功能改变

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The frequency and function of T cells, monocytes, and dendritic cell subsets were investigated in 12 patients after acute myocardial infarction (AMI)—(T0), 1 month after the episode (T1), and in 12 healthy individuals (HG). The cell characterization and the functional studies were performed by flow cytometry and by RT-PCR, after cell sorting. The most important findings at T0 moment, when compared with T1 and HG, were: a decrease in the frequency of IL-2-producing T cells; a lower frequency of TNF-α- and IL-6-producing monocytes, myeloid dendritic cells, and CD14−/lowCD16+DCs; and a lower TNF-α mRNA expression, after sorting these cells. Moreover, the regulatory function of Treg cells, at T0 moment, was upregulated, based on the FoxP3, CTLA-4, and TGF-β mRNA expression increase. The majority of these phenotypic and functional alterations disappeared at T1. Our data demonstrate that AMI induces a significant change in the immune system homeostasis.
机译:在12例急性心肌梗死(AMI)-(T0),发作后1个月(T1)和12例健康个体(HG)中研究了T细胞,单核细胞和树突状细胞亚群的频率和功能。细胞分选后,通过流式细胞仪和RT-PCR进行细胞表征和功能研究。与T1和HG相比,T0时刻最重要的发现是:产生IL-2的T细胞频率降低;产生TNF-α和IL-6的单核细胞,骨髓树突状细胞和CD14 -/ low CD16 + DC的频率较低;对这些细胞进行分选后,TNF-αmRNA的表达降低。此外,基于FoxP3,CTLA-4和TGF-βmRNA表达的增加,Treg细胞在T0时刻的调节功能被上调。这些表型和功能性改变中的大多数在T1时消失了。我们的数据表明,AMI诱导了免疫系统稳态的显着变化。

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