Synergistic effects of vascular IL-17 and TNFalpha may promote coronary artery disease.
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 TNFalpha is also up-regulated and recent studies suggest that cellular signaling pathways induced by IL-17 and TNFalpha converge. Recent studies showed that vascular endothelial and/or smooth muscle cells also express TNFalpha and IL-17, which can be up-regulated in pro-atherogenic pathophysiological conditions in the coronary arteries. TNFalpha 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 TNFalpha is much less understood. We propose that increased vascular IL-17 and TNFalpha levels can act synergistically to create a pro-inflammatory microenvironment promoting the development of atherosclerotic vascular disease.
Department of Physiology, New York Medical College, Valhalla, NY 10595, USA.
Anna
A
Csiszar
Zoltan
Z
Ungvari
D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D002986:Clinical Trials as Topic; D003324:Coronary Artery Disease / Q000276:immunology* / Q000378:metabolism; D019317:Evidence-Based Medicine; D006801:Humans; D020381:Interleukin-17 / Q000276:immunology* / Q000378:metabolism; D018448:Models, Immunological; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology* / Q000378:metabolism
D015415:Biomarkers; D020381:Interleukin-17; D014409:Tumor Necrosis Factor-alpha