Role of interleukin-10 in atherogenesis and plaque stabilization

Considerable progress has been made in the understanding of atherogenesis and atherosclerosis is now considered to be an inflammatory disease of the vessel wall involving several cell types, such as endothelial cells, smooth muscle cells and macrophages. Progression of an atheroslerotic lesion can lead to vulnerable and rupture-prone plaques, causing thrombus formation and the development of acute coronary syndromes. The balance between inflammatory (e.g., tumor necrosis factor-alpha, interleukin-6,) and anti-inflammatory cytokines (e.g., IL-10) seems to be of critical importance in the pathogenesis of plaque formation and destabilization, and it has recently been suggested that an inflammatory imbalance in unstable disease with inadequately raised IL-10 levels is also of importance. This lack of IL-10-mediated responses could promote inflammation, enhance oxidative stress and foam cell apoptosis, leading to plaque destabilization and thrombus formation and the development of acute coronary syndromes. Based on these issues, IL-10 has been postulated as an immunological scalpel in atherosclerotic disorders. Knowledge of IL-10 as a modulator of plaque stability may provide multiple opportunities for the treatment and prevention of atherosclerotic diseases in the future.