Inflammation and immune system interactions in atherosclerosis

Cell Mol Life Sci. 2013 Oct;70(20):3847-69. doi: 10.1007/s00018-013-1289-1. Epub 2013 Feb 21.

Abstract

Cardiovascular disease (CVD) is the leading cause of mortality worldwide, accounting for 16.7 million deaths each year. The underlying cause of the majority of CVD is atherosclerosis. In the past, atherosclerosis was considered to be the result of passive lipid accumulation in the vessel wall. Today's picture is far more complex. Atherosclerosis is considered a chronic inflammatory disease that results in the formation of plaques in large and mid-sized arteries. Both cells of the innate and the adaptive immune system play a crucial role in its pathogenesis. By transforming immune cells into pro- and anti-inflammatory chemokine- and cytokine-producing units, and by guiding the interactions between the different immune cells, the immune system decisively influences the propensity of a given plaque to rupture and cause clinical symptoms like myocardial infarction and stroke. In this review, we give an overview on the newest insights in the role of different immune cells and subtypes in atherosclerosis.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Adaptive Immunity
  • Antigen Presentation
  • Atherosclerosis / immunology
  • Atherosclerosis / metabolism
  • Atherosclerosis / pathology*
  • CD4-Positive T-Lymphocytes / immunology
  • CD4-Positive T-Lymphocytes / pathology
  • Cell Adhesion
  • Cell Communication*
  • Dendritic Cells / immunology
  • Dendritic Cells / pathology
  • Foam Cells / immunology
  • Foam Cells / pathology
  • Humans
  • Immunity, Innate
  • Inflammation / pathology*
  • Interferon-gamma / immunology
  • Lipid Metabolism
  • Monocytes / immunology
  • Monocytes / metabolism
  • Monocytes / pathology
  • Plaque, Atherosclerotic / metabolism
  • Plaque, Atherosclerotic / pathology*

Substances

  • Interferon-gamma