Innate and adaptive immune responses participate in atherosclerosis. Pentraxins, an essential component of the humoral arm of innate immunity, are a superfamily of acute phase proteins highly conserved during evolution and can be classified as short pentraxins such as C-reactive protein (CRP) and long pentraxins such as PTX3. The latter has an unrelated, long N-terminal domain coupled to the C-terminal pentraxin domain and differs from CRP in gene organization, cellular source, and recognized ligands. PTX3 in humans, like CRP, is a marker of atherosclerosis and correlates with the risk of developing vascular events. Although CRP sequence and regulation have not been conserved during evolution between mouse and man, the conservation of sequence, gene organization, and regulation of PTX3 in evolution enables one to address the question regarding its pathophysiologic roles in genetically modified mice. Deficiency of PTX3 is associated with increased heart damage with a greater no-reflow area and increased inflammatory response in a model of acute myocardial infarction (MI) caused by coronary artery ligation. More recently, deficiency of PTX3 on an apolipoprotein E knockout background was associated with increased atherosclerosis, macrophage accumulation within the plaque, and a more pronounced inflammatory profile in the vascular wall. Although these observations point to a cardiovascular protective effect of PTX3, they also suggest the possibility that the increased levels of PTX3 in subjects with cardiovascular disease (CVD) may reflect a protective physiologic response that correlates with the severity of the disease. In summary, data that are accumulating suggest that the increase of pentraxins in atherosclerosis could not be regarded as a harmful response but rather a further attempt to protection of our body.
Copyright (c) 2010 Elsevier Inc. All rights reserved.