Abstract
Atherosclerosis is the leading cause of death worldwide and leukocyte recruitment is a key element of this phenomenon, thus allowing immune cells to enter the arterial wall. There, in concert with accumulating lipids, the invading leukocytes trigger a plethora of inflammatory responses which promote the influx of additional leukocytes and lead to the continued growth of atherosclerotic plaques. The recruitment process follows a precise scheme of tethering, rolling, firm arrest, crawling and transmigration and involves multiple cellular and subcellular players. This review aims to provide a comprehensive up-to-date insight into the process of leukocyte recruitment relevant to atherosclerosis, each from the perspective of endothelial cells, monocytes and macrophages, neutrophils, T lymphocytes and platelets. In addition, therapeutic options targeting leukocyte recruitment into atherosclerotic lesions—or potentially arising from the growing body of insights into its precise mechanisms—are highlighted.
Highlights
Atherosclerosis is a chronic disease characterized by the accumulation of lipoprotein particles and inflammatory cells inside the arterial vessel wall of large- and medium-sized arteries
By following leukocytes step by step on their way into atherosclerotic plaques, it became clear that all leukocytes, differing in their affinity for specific adhesion molecules or chemokines, use the same overall concept of tethering and rolling, adhesion, crawling and transmigration
Rolling is mainly mediated by P-selectin glycoprotein ligand-1 (PSGL-1) and during rolling, chemokine-chemokine receptor interactions activate the high affinity conformation of leukocyte integrins in a process called inside-out signaling, paving the way for firm adhesion via very late antigen 4 (VLA-4) or lymphocyte function-associated antigen 1 (LFA-1)
Summary
Atherosclerosis is a chronic disease characterized by the accumulation of lipoprotein particles and inflammatory cells inside the arterial vessel wall of large- and medium-sized arteries. Atherosclerotic plaques may destabilize during the progression of the disease leading to plaque rupture/erosion resulting in partial or complete vessel obstruction which may cause cardiovascular events such as myocardial infarction (MI) or stroke [1]. Evidence accumulated highlighting the contribution of immune cells in the etiology of atherosclerosis [4]. Leukocytes, the effector cells of the immune system, contribute to all stages of the disease. Monocyte-derived macrophages, neutrophils and T lymphocytes are involved in inflammatory processes inside the vessel wall during lesion initiation, progression and rupture [5, 6]. We aim to summarize basic concepts of leukocyte recruitment and highlight novel findings in the context of atherosclerosis
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