Linking immunity to atherosclerosis: implications for vascular pharmacology--a tribute to Göran K. Hansson

Abstract

For the past decade, we have deepened our understanding of the pathogenesis of atherosclerosis, a chronic arterial disease that causes cardiac and cerebral infarction and peripheral vascular disorders. Because of this extended understanding, more effective strategies for prevention and treatment of this disease are emerging. One of the fundamental mechanisms that lead to progress or regression in atherosclerosis, thus influencing its life-threatening complications, occurs through functional changes in vascular immunity and inflammation. This review briefly summarizes the discoveries in basic and translational sciences in this area and recent advances in clinical medicine against atherosclerotic vascular diseases.

Figure 1

Immunofluorescence of human HLA-DR antigens at the edge of a human carotid atherosclerotic plaque. Strong green immunofluorescent staining of HLA-DR was found in the majority of vascular cells in the plaque tissue (Jonasson et al. J Clin Invest. 1985 Jul;76:125–31, with permission).

Figure 2. Schematic demonstration of atherogenic low density lipoprotein (LDL) and immune cell infiltration in atherosclerotic lesions

During the development of atherosclerosis, monocytes infiltrate the arterial intima where they differentiate into macrophages and take up modified LDL particles. T cells also enter the lesions and become activated when they encounter antigen-presenting cells, such as dendritic cells and macrophages.