Inflammation and the pathogenesis of atherosclerosis.

The notion that inflammation contributes to atherosclerosis has now gained considerable currency. Inflammation participates in atherosclerosis inception, progression, and thrombotic complications. Induced expression of endothelial leukocyte adhesion molecules and chemoattractant cytokines recruit blood cells to the arterial intima. Lesions can contain virtually every type of leukocyte. Monocytes mature into macrophages and imbibe lipids becoming foam cells, a hallmark of the atherosclerotic lesion. T lymphocytes can instruct the more numerous macrophages to express genes involved in the progression of the atheroma and its eventual destabilization. Inflammation is becoming clinically actionable to refine risk prediction, allocate treatments, and as a therapeutic target.