Leukocyte influx in atherosclerosis

Curr Drug Targets. 2007 Dec;8(12):1239-48. doi: 10.2174/138945007783220650.

Abstract

Atherosclerosis is a chronic inflammatory disease of the arterial wall and an increasing body of evidence suggests that the immune system actively participates in the initiation, progression and persistence of atherosclerosis. Different types of leukocytes such as T and B lymphocytes, natural killer cells (NK) and NKT cells, macrophages, dendritic cells and mast cells have been found within atherosclerosis-prone aortas. The mechanisms of monocyte recruitment have been partially characterized and involve P-selectin, E-selectin, VCAM-1, ICAM-1 and JAM-A. CXCL1, CCL5, CXCL4, CXCL7 and MIF are also implicated in monocyte trafficking into aortas. Recently it has been reported that Ly6C(high) and Ly6C(low) monocyte subsets differently use CCL2, CX3CL1 and CCL5 for their homing into atherosclerotic aortas. T and B lymphocytes constitutively migrate into the normal and atherosclerotic aortic wall in an L-selectin-dependent manner. Recent studies suggest an important role of CCL5, CXCL10, CXCL16, CXCR6 and MIF in T cell influx into the atherosclerotic wall. However, there is little information available on the mechanisms of recruitment of other types of the immune cells such as NK, NKT and mast cells. In this review we shall summarize what is known about leukocyte recruitment into the aortic wall during atherosclerosis with a focus on mouse model systems.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Aorta / immunology*
  • Aorta / pathology
  • Atherosclerosis / immunology*
  • Atherosclerosis / physiopathology
  • Chemokines / immunology
  • Chemokines / metabolism
  • Disease Models, Animal
  • Leukocytes / immunology*
  • Leukocytes / metabolism
  • Mice
  • Receptors, Chemokine / immunology
  • Receptors, Chemokine / metabolism

Substances

  • Chemokines
  • Receptors, Chemokine