NDLI: Interleukin-17 stimulates inducible nitric oxide synthase-dependent toxicity in mouse beta cells

Content Provider	Springer Nature Link
Author	Miljkovic, D. Cvetkovic, I. Momcilovic, M. Maksimovic Ivanic, D. Stosic Grujicic, S. Trajkovic, V.
Copyright Year	2005
Abstract	The influence of the proinflammatory cytokine interleukin (IL)-17 on inducible nitric oxide (NO) synthase (iNOS)-mediated NO release was investigated in the mouse insulinoma cell line MIN6 and mouse pancreatic islets. IL-17 markedly augmented iNOS mRNA/protein expression and subsequent NO production induced in MIN6 cells or pancreatic islets by different combinations of interferon-γ, tumor necrosis factor-α, and IL-1β. The induction of iNOS by IL-17 was preceded by phosphorylation of p38 mitogen-activated protein kinase (MAPK), and inhibition of p38 MAPK activation completely abolished IL-17-stimulated NO release. IL-17 enhanced the NO-dependent toxicity of proinflammatory cytokines toward MIN6 cells, while IL-17-specific neutralizing antibody partially reduced the NO production and rescued insulinoma cells and pancreatic islets from NO-dependent damage induced by activated T cells. Finally, a significant increase in blood IL-17 levels was observed in a multiple low-dose streptozotocin model of diabetes, suggesting that T cell-derived IL-17 might be involved in NO-dependent damage of beta cells in this disease.
Starting Page	2658
Ending Page	2668
Page Count	11
File Format	PDF
ISSN	1420682X
Journal	Cellular and Molecular Life Sciences
Volume Number	62
Issue Number	22
e-ISSN	14209071
Language	English
Publisher	Birkhäuser-Verlag
Publisher Date	2005-11-02
Publisher Place	Basel
Access Restriction	Subscribed
Subject Keyword	IL-17 iNOS nitric oxide beta cells T cells autoimmunity diabetes Cell Biology Biomedicine general Life Sciences Biochemistry
Content Type	Text
Resource Type	Article
Subject	Cell Biology Molecular Biology Molecular Medicine Pharmacology Cellular and Molecular Neuroscience

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