Abstract
Atherosclerosis is the major cause of the development of cardiovascular disease, which, in turn, is one of the leading causes of mortality worldwide. From the point of view of pathogenesis, atherosclerosis is an extremely complex disease. A huge variety of processes, such as violation of mitophagy, oxidative stress, damage to the endothelium, and others, are involved in atherogenesis; however, the main components of atherogenesis are considered to be inflammation and alterations of lipid metabolism. In this review, we want to focus on inflammation, and more specifically on the cellular elements of adaptive immunity, T and B cells. It is known that various T cells are widely represented directly in atherosclerotic plaques, while B cells can be found, for example, in the adventitia layer. Of course, such widespread and well-studied cells have attracted attention as potential therapeutic targets for the treatment of atherosclerosis. Various approaches have been developed and tested for their efficacy.
Highlights
Cardiovascular disease (CVD) is the most widespread cause of death
These cells participate in the chronic inflammatory process, which typically occurs within the arterial wall [6]
We recently demonstrated that low-dose treatment with ibrutinib leads to margin zone lowering and is linked with an increase in the number of FOB cells [88]
Summary
Cardiovascular disease (CVD) is the most widespread cause of death. In 2013, 7.3 million people died because of CVD, which, according to world statistics, is 31.5% of total deaths [1]. By remaining in the plaque, the cholesterol foam cells absorb lipids and stimulate the progression of the disease, developing a chronic inflammatory response [5]. Macrophages and monocytes are part of the innate immune system, which plays an essential role in the preservation of immune homeostasis by eliminating infectious agents and stimulating tissue damage repair In atherosclerosis, these cells participate in the chronic inflammatory process, which typically occurs within the arterial wall [6]. The type of antigen, T-cell receptor signal intensity, and the local cytokine environment define the Th subsets into which T-cell can differentiate. These factors mediate Th polarization in atherosclerotic lesions [7].
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