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

Abstract

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. 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. 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). 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.