scholarly journals Model IgG Monoclonal Autoantibody–Anti-Idiotype Pair for Dissecting the Humoral Immune Response to Oxidized Low Density Lipoprotein

Hybridoma ◽  
2012 ◽  
Vol 31 (2) ◽  
pp. 87-98 ◽  
Author(s):  
Shang-Hung Chang ◽  
Michael Johns ◽  
Joseph J. Boyle ◽  
Ellen McConnell ◽  
Paul A. Kirkham ◽  
...  
Keyword(s):  
Immune Response ◽  
Humoral Immune Response ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Oxidized Low Density Lipoprotein ◽  
Humoral Immune ◽  
Monoclonal Autoantibody

LOX-1, oxidant stress, mtDNA damage, autophagy, and immune response in atherosclerosis

2014 ◽  
Vol 92 (7) ◽  
pp. 524-530 ◽  
Author(s):  
Zufeng Ding ◽  
Shijie Liu ◽  
Xianwei Wang ◽  
Yao Dai ◽  
Magomed Khaidakov ◽  
...  
Keyword(s):  
Immune Response ◽  
Dna Damage ◽  
Mitochondrial Dna ◽  
Oxidant Stress ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Oxidized Low Density Lipoprotein ◽  
Mitochondrial Dna Damage ◽  
Monocyte Migration

As a major receptor for oxidized low density lipoprotein (ox-LDL), lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) is upregulated in many pathophysiological events, including endothelial cell dysfunction and smooth muscle cell growth, as well as monocyte migration and transformation into foam cells, which are present in atherosclerosis and myocardial ischemia. Excessive production of reactive oxygen species (ROS) increases LOX-1 expression, induces mitochondrial DNA damage, and activates autophagy. Damaged mitochondrial DNA that escapes from autophagy induces an inflammatory response. This paper reviews the potential link between LOX-1, mitochondrial DNA damage, autophagy, and immune response in atherosclerosis.

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