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DOI 10.1016/j.atherosclerosis.2011.03.043

Медицинская библиотека · Atherosclerosis · 2011

Activation of Th17/Th1 and Th1, but not Th17, is associated with the acute cardiac event in patients with acute coronary syndrome.

Zhao Zhao, Wu Yue, Cheng Manli, Ji Yuqiang, Yang Xiaobo, Liu Ping, Jia Shaobin, Yuan Zuyi

СтатьяПоддержка исследования: вне правительства СШАПеревод пока не подготовлен

Аннотация

OBJECTIVE

Th1 activation and regulatory T (Treg) cell suppression have been observed in acute coronary syndrome (ACS), including unstable angina (UA) and acute myocardial infarction (AMI). However, the role of Th17 cell or IL-17A remains controversial in ACS patients, and little is known about the role of recently discovered Th17/Th1 cells, a subset of Th17 cells, in coronary artery disease (CAD). The purpose of this study is to investigate functional changes of Th17/Th1, Th17, Th1, Th2 and Treg cells in ACS patients.

METHODS

The contents of Th17/Th1, Th17, Th1, Th2 and Treg cells, related gene expression, and plasma cytokines from CAD and control patients with normal coronary arteries (NCA) were measured by flow cytometry, real-time quantitative PCR and ELISA.

RESULTS

Th17/Th1 and Th1 cell contents and related gene expression (T-bet, IFN-γ, STAT4, RORγt, STAT3 and IL-17) were significantly increased in ACS patients, whereas plasma IFN-γ only increased in CAD patients. In contrast, Treg cell population, Foxp3 levels, and plasma TGF-β1 were decreased in ACS patients compared with stable angina (SA) and NCA patients.

CONCLUSION

The study showed activation of Th17/Th1 and Th1 cell in ACS patients, which may provide insight into the mechanisms underlying culprit plaque relevant T-cell activation in ACS patients.

Для цитирования: Zhao Zhao, Wu Yue, Cheng Manli, Ji Yuqiang, Yang Xiaobo, Liu Ping, Jia Shaobin, Yuan Zuyi. Activation of Th17/Th1 and Th1, but not Th17, is associated with the acute cardiac event in patients with acute coronary syndrome.. Atherosclerosis. 2011. DOI: 10.1016/j.atherosclerosis.2011.03.043.

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