Abstract
Atherosclerosis is a chronic process associated with arterial inflammation, the accumulation of lipids, plaque formation in vessel walls, and thrombosis with late mortal complications such as myocardial infarction and ischemic stroke. Immune and inflammatory responses have significant effects on every phase of atherosclerosis. Increasing evidence has shown that both innate and adaptive “arms” of the immune system play important roles in regulating the progression of atherosclerosis. Accumulating evidence suggests that a unique type of innate immune cell, termed dendritic cells (DCs), play an important role as central instigators, whereas adaptive immune cells, called T lymphocytes, are crucial as active executors of the DC immunity in atherogenesis. These two important immune cell types work in pairs to establish pro-atherogenic or atheroprotective immune responses in vascular tissues. Therefore, understanding the role of DCs and T cells in atherosclerosis is extremely important. Here, in this review, we will present a complete overview, based on existing knowledge of these two cell types in the atherosclerotic microenvironment, and discuss some of the novel means of targeting DCs and T cells as therapeutic tactics for the treatment of atherosclerosis.
Highlights
The term “atherosclerosis” is derived from the Greek word “atheroma” meaning “soft or porridgelike” to describe the physical appearance of the intima of arteries, which was first named by Felix Marchand in 1904 to account for almost all obstructive processes in the arteries [1]
This abnormal deposition of lipids on the arterial wall initiates the recruitment of leukocytes and accumulation of oxidized low-density lipoprotein (LDL) within the intima of arteries
In contrast to immature dendritic cells (DCs), ApoE−/− mice receiving mature GM-DCs loaded with the modified autoantigen, MDA-LDL, suffered from aggravated atherosclerosis with a 40% increase in lesion size, augmented vascular cell adhesion molecule 1 (VCAM-1) expression, and increased MDA-LDL-specific IgG/immunoglobulin M (IgM) levels, but no induced Tregs [167]
Summary
The term “atherosclerosis” is derived from the Greek word “atheroma” meaning “soft or porridgelike” to describe the physical appearance of the intima of arteries, which was first named by Felix Marchand in 1904 to account for almost all obstructive processes in the arteries [1]. Being one of the leading causes of morbidity and death from cardiovascular diseases [2], atherosclerosis involves a chronic inflammatory process within the large and medium-sized arterial walls that leads to characteristic plaque formation, rupture, and ischemic injury of the dependent vascular bed [3, 4]. As a result, this tissue damage will further trigger immune responses. This abnormal deposition of lipids on the arterial wall initiates the recruitment of leukocytes and accumulation of oxidized LDL (oxLDL) within the intima of arteries
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