Correlation of apolipoprotein A-I with T cell subsets and interferon-ү in coronary artery disease

载脂蛋白AI与冠状动脉疾病中T细胞亚群和干扰素-γ的相关性

阅读:1
作者:Xinlin Xiong ,Zonggang Duan ,Haiyan Zhou ,Guangwei Huang ,Li Niu ,Zhenhua Luo ,Wei Li

Abstract

Background: The association of Apolipoprotein A-I (APOAI) with T cell subsets and interferon-ү (IFN-γ) in patients with coronary artery disease (CAD) has been not reported. Thus, this study aimed to investigate the association of APOAI with T cell subsets and IFN-γ in CAD. Methods: This study included a total of 107 patients with CAD including acute coronary syndrome and chronic coronary syndrome. T cell subsets, and CD3-CD56+ natural killer cells were quantified by flow cytometric analysis. The serum concentrations of IFN-ү were measured by enzyme-linked immunosorbent assay. Lipid profiles, C-reactive protein (CRP), and fibrinogen were measured in the clinical laboratory. Clinical data was obtained duration hospitalization. Results: The CD4+ T cells were higher in patients of the low-APOAI group (<median: 1.2 mmol/L) than in patients of the high-APOAI group(≥median: 1.2 mmol/L) (p < .05). The CD8+ T cells were lower in patients of the low APOAI group than in patients of the high-APOAI group (p < .05). APOAI was inversely associated with CD4+ T cells, IFN-γ, and was positively associated with CD8+ T cells (p < .05). No correlation was observed between CD3 + CD56+ cells, regulatory T cells (Tregs), and CD3-CD56+ natural killer cells and APOAI (p > .05). The high-density lipoprotein cholesterol (HDL-C) was also inversely associated with CD4+ T cells (p < .05), and positively associated with CD8+ T cells (p < .05). Lastly, APOA1 and HDL-C did not correlated with fibrinogen and CRP (p > .05). Conclusion: The present study demonstrated the correlation of APOAI with T cell subsets and IFN-γ in CAD. These results provided novel information for the regulatory action between APOAI and T cell subsets and inflammatory immunity in CAD.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。