title: Monocyte and macrophage dynamics during atherogenesis.
abstract: Vascular inflammation is associated with and in large part driven by changes in the leukocyte compartment of the vessel wall. Here, we focus on monocyte influx during atherosclerosis, the most common form of vascular inflammation. Although the arterial wall contains a large number of resident macrophages and some resident dendritic cells, atherosclerosis drives a rapid influx of inflammatory monocytes (Ly-6C(+) in mice) and other monocytes (Ly-6C(-) in mice, also known as patrolling monocytes). Once in the vessel wall, Ly-6C(+) monocytes differentiate to a phenotype consistent with inflammatory macrophages and inflammatory dendritic cells. The phenotype of these cells is modulated by lipid uptake, Toll-like receptor ligands, hematopoietic growth factors, cytokines, and chemokines. In addition to newly recruited macrophages, it is likely that resident macrophages also change their phenotype. Monocyte-derived inflammatory macrophages have a short half-life. After undergoing apoptosis, they may be taken up by surrounding macrophages or, if the phagocytic capacity is overwhelmed, can undergo secondary necrosis, a key event in forming the necrotic core of atherosclerotic lesions. In this review, we discuss these and other processes associated with monocytic cell dynamics in the vascular wall and their role in the initiation and progression of atherosclerosis.
authors.affiliation: Division of Inflammation Biology, La Jolla Institute for Allergy and Immunology, La Jolla, CA 92037, USA. klaus@liai.org
authors.forename: Klaus
authors.initials: K
authors.lastname: Ley
authors.forename: Yury I
authors.initials: YI
authors.lastname: Miller
authors.forename: Catherine C
authors.initials: CC
authors.lastname: Hedrick
mesh_terms: D000818:Animals; D017209:Apoptosis; D050197:Atherosclerosis / Q000276:immunology* / Q000473:pathology; D018450:Disease Progression; D005487:Foam Cells / Q000276:immunology; D006801:Humans; D007249:Inflammation / Q000276:immunology* / Q000473:pathology; D018836:Inflammation Mediators / Q000378:metabolism; D050356:Lipid Metabolism; D008264:Macrophages / Q000276:immunology* / Q000473:pathology; D009000:Monocytes / Q000276:immunology* / Q000473:pathology; D009336:Necrosis; D010641:Phenotype; D015398:Signal Transduction
chemical_list: D018836:Inflammation Mediators