Immunity in Atherosclerosis: Focusing on T and B Cells

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.

Keywords: B cells; CVD; T cells; atherosclerosis; immunity.

Figure 1

Various types of T cells are attracted to the atherosclerotic lesion site by the chemokines released by the activated endothelial cells. IFNγ (interferon-gamma) is produced by Th1 cells and has proatherogenic features. It inhibits the proliferation of smooth muscle cells, decreases collagen production, and activates macrophages. IL-4 (interleukin-4) is produced by Th2 cells and has atheroprotective effects mediated by the ability to inhibit Th1 cells. Granzyme B and perforin, which are released by CD4⁺CD28nullT-cells can damage vascular wall cells. CD8⁺ T-cells produce proatherogenic IFNγ or cause an atheroprotective effect via decreasing macrophage content in the plaque. Treg cells release TGF-β (transforming growth factor β), contributing to Th1 and Th17 response inhibition, as well as enhancing smooth muscle cell proliferation. NK-T cells are potentially involved in the destabilization of atherosclerotic plaques. No exact roles for Th17 and γδ T-cells, which are present in plaque, have yet been established.