| | In humans, atherosclerotic plaques contain blood-borne inflammatory and immune cells (~40% of cells present within the plaques express macrophage markers, ~10% are CD3+ T cells) as well as endothelial cells, smooth muscle cells, extracellular matrix proteins, lipids and acellular lipid-rich debris. Small populations of mast cells, B cells and dendritic cells (DCs) are also present in plaques and, together with T cells, monocytes and macrophages, might traffic between the blood, the atherosclerotic lesion and the regional lymph nodes. Many of these immune cells show signs of activation and produce proinflammatory cytokines, including interferon-γ (IFNγ) and tumour-necrosis factor (TNF).
Inflammation is induced by innate immunity and adaptive immunity. The two arms of the immune response can either promote or attenuate atherosclerosis. Recent studies suggest that subtypes of T cells, called regulatory T cells, previously shown to maintain immunologic tolerance to self and nonself antigens, are powerful inhibitors of atherosclerosis (Ait-Oufella et al, Nature Medecine, 2006).
Mediators in atherogenesis
Pathogenic and regulatory immunity in atherosclerosis Candidate antigens [oxidized lipoproteins (oxLDL), heat shock proteins (HSP), phosphorylcholine (PC), apoptotic bodies. . . ] from the plaque are taken up by Antigen Presenting Cells (APC) and may induce Tcell responses. Maturation of APC is necessary for T-cell priming. |