Synergistic effects of vascular IL-17 and TNFα may promote coronary artery disease

Abstract 

Interleukin (IL)-17 is a pro-inflammatory cytokine originally described in T lymphocytes. Increased production of IL-17 has been linked to the induction of cytokines, chemokines and adhesion molecules in various cell types, effects that likely contribute to a number of inflammatory diseases including rheumatoid arthritis. Importantly, in the same pathophysiological conditions production of TNFα is also up-regulated and recent studies suggest that cellular signaling pathways induced by IL-17 and TNFα converge. Recent studies showed that vascular endothelial and/or smooth muscle cells also express TNFα and IL-17, which can be up-regulated in pro-atherogenic pathophysiological conditions in the coronary arteries. TNFα has been shown to exert pro-inflammatory vascular effects (e.g., induction of oxidative stress, endothelial apoptosis, up-regulation of adhesion molecules and chemokines), however, the role of vascular IL-17 and its interaction with TNFα is much less understood. We propose that increased vascular IL-17 and TNFα levels can act synergistically to create a pro-inflammatory microenvironment promoting the development of atherosclerotic vascular disease.