Abstract.
The effect of interleukin (IL)-17 on the activation of inducible nitric oxide (NO) synthase (iNOS) and subsequent production of NO was investigated. IL-17 induced NO production in both mouse and rat endothelial cells in a dose- and time-dependent manner. This was paralleled by the induction of mRNA for iNOS, which was markedly down-regulated by specific antagonists of protein tyrosine kinase, p38 MAP kinase or iNOS transcription factor NF-κB. The expression of iNOS transcription factor IRF-1 was also induced by IL-17 and blocked by all three inhibitors, suggesting that the induction of iNOS by IL-17 might be partly exerted through IRF-1 activation. Neutralization with the specific antibody showed that endogenous IL-17 is involved in T cell-mediated NO production in endothelial cells and NO-dependent suppression of T cell growth. These data indicate that IL-17-triggered iNOS activation in endothelial cells might participate in regulation of the T cell-dependent inflammatory response.
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Received 6 November 2002; received after revision 11 December 2002; accepted 13 January 2003
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Miljkovic, D., Cvetkovic, I., Vuckovic, O. et al. The role of interleukin-17 in inducible nitric oxide synthase-mediated nitric oxide production in endothelial cells. CMLS, Cell. Mol. Life Sci. 60, 518–525 (2003). https://doi.org/10.1007/s000180300043
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DOI: https://doi.org/10.1007/s000180300043