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 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.
journal_name
Med Hypothesesjournal_title
Medical hypothesesauthors
Csiszar A,Ungvari Zdoi
10.1016/j.mehy.2004.03.009keywords:
subject
Has Abstractpub_date
2004-01-01 00:00:00pages
696-8issue
4eissn
0306-9877issn
1532-2777pii
S0306987704002191journal_volume
63pub_type
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