Abstract
Cardiac and cerebrovascular accidents represent one of the two leading causes of death. The role of inflammation in the basic lesion of the vessels - the atheromatous plaque - is now well known. The mechanisms of plaque formation, rupture - source of vascular accidents - and control, or even resolution, are complex and still poorly understood. The lecture took stock of current knowledge and questions. The respective roles of cholesterol-rich lipoproteins in the activation of endothelial cells, then platelets, neutrophils, mast cells and T and B lymphocytes were described. In particular, the accumulation of pro-inflammatory macrophages through infiltration of the vascular wall and in situ proliferation is an essential element in the genesis and persistence of atheromatous lesions. These macrophages are deficient in the non-inflammatory elimination of dead cells by the efferocytosis mechanism. Activation of macrophages by oxidized phospholipids could account for this situation. The physiological mechanisms by which atheromatous plaque resolution can be brought into play were also discussed, highlighting the heterogeneity and different functional states of macrophages present in lesions, well highlighted by single-cell analyses of mRNA and protein expression profiles.
