The in and out of monocytes in atherosclerotic plaques: Balancing inflammation through migration

Recent clinical and experimental evidence indicates that inflammatory processes in the vascular wall are the decisive factor that accounts for the rate of lesion formation and clinical development in patients suffering from atherosclerosis (1). The response-to-injury hypothesis (2) predicts that particular stimuli (= injury) trigger the initiation of an inflammatory cascade in the vessel wall. In addition, alteration of the lipid metabolism is a critical factor intertwined with the complex inflammatory reactions that occur during lesion development. The progressive accumulation of macrophages and other immune cells in the atherosclerotic plaque is one of the hallmarks in atherogenesis (Fig. 1). The ins and outs of macrophage precursors, the blood monocyte, in atherosclerotic lesions have been elegantly dissected in a study by Llodra et al. (3) in this issue of PNAS. The authors suggest that not only recruitment of monocytes to but also their retention within the atherosclerotic lesion contributes to the progression of plaque development.