Abstract
Atherosclerosis is a chronic inflammatory disease that is initiated by the deposition and accumulation of low-density lipoproteins in the artery wall. In this review, we will discuss the role of T- and B-cells in human plaques at different stages of atherosclerosis and the utility of profiling circulating immune cells to monitor atherosclerosis progression. Evidence supports a proatherogenic role for intraplaque T helper type 1 (Th1) cells, CD4+CD28null T-cells, and natural killer T-cells, whereas Th2 cells and regulatory T-cells (Treg) have an atheroprotective role. Several studies indicate that intraplaque T-cells are activated upon recognition of endogenous antigens including heat shock protein 60 and oxidized low-density lipoprotein, but antigens derived from pathogens can also trigger T-cell proliferation and cytokine production. Future studies are needed to assess whether circulating cellular biomarkers can improve identification of vulnerable lesions so that effective intervention can be implemented before clinical manifestations are apparent.
Highlights
Atherosclerosis is a chronic vascular disease involving endothelial dysfunction following the deposition and accumulation of lipoproteins (e.g., low-density lipoproteins (LDL)) in the arterial intima
This study revealed a role for chemokine signaling through CXCR3 in promoting recruitment and homing of T helper 1 (Th1) cells to the site of plaque development
These findings suggest that CD4+CD28null T-cells may damage cells in the vascular wall, thereby affecting the stability of plaques
Summary
Atherosclerosis is a chronic vascular disease involving endothelial dysfunction following the deposition and accumulation of lipoproteins (e.g., low-density lipoproteins (LDL)) in the arterial intima. Cells of the innate and adaptive immune system are present in the different layers (intima, media, and adventitia) of the artery walls throughout the development of atherosclerotic plaques in mice and humans [3,4]. It is well established that different subsets of monocytes and macrophages play a crucial role in the atherosclerotic plaque establishment and disease progression [4]. Human regulatory T-cells (Treg) can suppress the activation of immune cells through cell-to-cell contact and/or the secretion of inhibitory cytokines (e.g., transforming growth factor (TGF)-β and IL-10) [6]. They are characterized by the expression of the transcription factor forkhead box P3 (FOXP3) and the IL-2 receptor α subunit, CD25
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