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

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.