Published online Apr 16, 2015. doi: 10.12998/wjcc.v3.i4.345
Peer-review started: May 13, 2014
First decision: June 6, 2014
Revised: December 1, 2014
Accepted: January 18, 2015
Article in press: January 20, 2015
Published online: April 16, 2015
Processing time: 334 Days and 22.9 Hours
Atherosclerosis is a chronic inflammatory disease arising from lipids, specifically low-density lipoproteins, and leukocytes. Following the activation of endothelium with the expression of adhesion molecules and monocytes, inflammatory cytokines from macrophages, and plasmacytoid dendritic cells, high levels of interferon (IFN)-α and β are generated upon the activation of toll-like receptor-9, and T-cells, especially the ones with Th1 profile, produce pro-inflammatory mediators such as IFN-γ and upregulate macrophages to adhere to the endothelium and migrate into the intima. This review presents an exhaustive account for the role of immune cells in the atherosclerosis.
Core tip: Activated endothelium to adhere to the endothelium and move into the intima with the expression of adhesion molecules appears to be an early event in atherosclerosis, which allows mononuclear leukocytes such as monocytes and T-cells. This inflammatory mechanism must be explained before determining a new therapy.