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急性心肌梗死后炎症外周血细胞的表型和功能改变。

Phenotypic and functional alterations on inflammatory peripheral blood cells after acute myocardial infarction.

机构信息

Histocompatibility Centre of Coimbra, Edifício São Jerónimo, 4° Piso, Praceta Mota Pinto, 3001-301 Coimbra, Portugal.

出版信息

J Cardiovasc Transl Res. 2012 Jun;5(3):309-20. doi: 10.1007/s12265-012-9365-8. Epub 2012 Apr 21.

Abstract

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(-/low)CD16(+)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.

摘要

研究了 12 例急性心肌梗死(AMI)患者(T0 时)、发病后 1 个月(T1 时)和 12 例健康个体(HG)的 T 细胞、单核细胞和树突状细胞亚群的频率和功能。通过流式细胞术和 RT-PCR 在细胞分选后进行细胞特征分析和功能研究。与 T1 和 HG 相比,T0 时的最重要发现为:产生 IL-2 的 T 细胞频率降低;产生 TNF-α 和 IL-6 的单核细胞、髓样树突状细胞和 CD14(-/low)CD16(+)DC 的频率降低;分选这些细胞后 TNF-α mRNA 表达降低。此外,基于 FoxP3、CTLA-4 和 TGF-β mRNA 表达增加,T0 时 Treg 细胞的调节功能上调。这些表型和功能改变中的大多数在 T1 时消失。我们的数据表明,AMI 诱导免疫系统稳态发生重大变化。

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