Abstract
In this overview to a new thematic series on the immune system and atherogenesis, I provide a very brief summary of current conceptions of atherogenesis, of the innate and adaptive immune systems, and of the participation of the latter in atherogenesis, with particular emphasis on studies of the involvement of the immune system in atherosclerosis reported in the last 2 years. This is followed by a short outline of the eight reviews that will make up this thematic series. The overview is concluded with some caveats that should be considered in the analysis of atherosclerosis in experimental animals.
Highlights
In this overview to a new thematic series on the immune system and atherogenesis, I provide a very brief summary of current conceptions of atherogenesis, of the innate and adaptive immune systems, and of the participation of the latter in atherogenesis, with particular emphasis on studies of the involvement of the immune system in atherosclerosis reported in the last 2 years
Supplementary key words innate immunity. This issue inaugurates a new Thematic Series that highlights the role of immune function in atherosclerosis
The expression of this pair was thought to be restricted to B-cells, dendritic cells, and activated T-cells, it is clear that they are more widely expressed in the cells present in atherosclerotic plaques. Interdiction of their interaction results in a reduction in lesion development, while modifying the composition of the lesion toward a less inflammatory and more fibrogenic lesion phenotype [31]. Another pair of costimulatory molecules that belong to the tumor necrosis factor (TNF) superfamily is LIGHT (TNFSF 14) [32] and its receptor, either HVEM (TNFRSF 14) expressed on lymphocytes and natural killer (NK) cells or lymphotoxin  expressed on stromal cells and monocytes [33]
Summary
It is widely recognized that atherosclerosis is a specific example of a chronic inflammatory response mainly to dyslipidemia and other risk factors. Oxidized phospholipid moieties of oxidized lipoproteins signal to many of the cells in the evolving plaque, especially to the endothelium overlying the accumulating OxLDL and to foam cells Among other responses, this signaling increases the expression of adhesion molecules that facilitate the homing of monocytes and lymphocytes to this localized activated endothelium. The progression of the lesion from the fatty xanthoma to a more complex lesion is characterized by the migration of smooth muscle cells from the media into the subendothelial intima and their subsequent proliferation This is mediated, in part, by the growth factors secreted from macrophage foam cells. The increase in the size of the evolving atherosclerotic plaque arises from the continued recruitment of monocytes and lymphocytes, the continued migration and proliferation of smooth muscle cells, the evolution of a necrotic core, and matrix protein synthesis. Activation of the macrophages in the lesions, on the lesion shoulders, may lead to the release of proteases, with disruption of the plaque surface giving rise to the unstable plaque lesion becoming the nidus for thrombosis and consequent clinical complications
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