Abstract
Atherosclerosis is the pathological basis of many cardiovascular and cerebrovascular diseases. The development of gene chip and high-throughput sequencing technologies revealed that the immune microenvironment of coronary artery disease (CAD) in high-risk populations played an important role in the formation and development of atherosclerotic plaques. Three gene expression datasets related to CAD were assessed using high-throughput profiling. CIBERSORT analysis revealed significant differences in five types of immune cells: activated dendritic cells (DCs), T follicular helper cells (Tfhs), resting CD4+ T cells, regulatory T cells (Tregs), and γδ T cells. Immune transcriptome analysis indicated higher levels of inflammatory markers (cytolytic activity, antigen presentation, chemokines, and cytokines) in the cases than in the controls. The level of activated DCs and the lipid clearance signaling score were negatively correlated. We observed a positive correlation between the fraction of Tfhs and lipid biosynthesis. Resting CD4+ T cells and the activity of pathways related to ossification in bone remodeling and glutathione synthesis showed a negative correlation. Gamma delta T cells negatively correlated with IL-23 signaling activity. GSEA revealed a close association with the inflammatory immune microenvironment. The present study revealed that CAD patients may have an inflammatory immune microenvironment and provides a timely update on anti-inflammatory therapies under current investigation.
Highlights
Coronary artery disease (CAD) leads to myocardial infarction (MI), ischemic cardiomyopathy, and arrhythmia, and it is the main source of cardiovascular morbidity, mortality, and the economic health burden worldwide [1]
The CIBERSORT algorithm was used to calculate the proportion of 22 immune cells based on the expression data of the discovery dataset (GSE40231; Figure 1B)
The coronary artery disease (CAD) group had fewer regulatory T cells (Tregs), γδ T cells, and resting CD4+ T cells (Figure 1C) than the control group. These results suggest that CAD exhibits inflammatory microenvironment patterns
Summary
Coronary artery disease (CAD) leads to myocardial infarction (MI), ischemic cardiomyopathy, and arrhythmia, and it is the main source of cardiovascular morbidity, mortality, and the economic health burden worldwide [1]. The past decade of research has provided a deeper understanding of the pathogenesis and treatment of CAD [2]. Despite this success, little progress has been made on elucidating the function of the immune microenvironment and its therapeutic Implications [3]. High-throughput sequencing technologies examine the role of the immune microenvironment of CAD in high-risk populations in the formation and development of atherosclerotic plaques (APs) [4, 9,10,11,12]. A growing number of studies indicate that cardiovascular events are determined by multiple biological processes that require different tailored therapeutic approaches, and future therapies for CAD should tackle the residual inflammatory process that statin therapy only partially addresses [13]. Pre-clinical studies revealed that the inhibition of IL-6 or its receptor achieved atheroprotective effects [17, 18]
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