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IL-17 potentiates neuronal injury induced by oxygen-glucose deprivation and affects neuronal IL-17 receptor expression.

Authors :
Wang DD
Zhao YF
Wang GY
Sun B
Kong QF
Zhao K
Zhang Y
Wang JH
Liu YM
Mu LL
Wang DS
Li HL
Source :
Journal of neuroimmunology [J Neuroimmunol] 2009 Jul 25; Vol. 212 (1-2), pp. 17-25. Date of Electronic Publication: 2009 May 19.
Publication Year :
2009

Abstract

Interleukin-17 (IL-17) is active in a variety of brain injuries, including ischemia. The objective of this study was to test the hypothesis that IL-17 potentiates neuronal injury after stroke. Increased expression of IL-17 and IL-17 receptor (IL-17R) in serum and cortex was evaluated by ELISA, RT-PCR and immunohistochemistry. In the in vitro model of oxygen-glucose deprivation (OGD), IL-17 showed a dose-dependent effect in promoting neuronal injury through IL-17-IL-17R combination which can be blocked by IL-17R/Fc chimera. Our results demonstrated the up-regulation of IL-17 and IL-17R following permanent middle cerebral artery occlusion and suggested that they contributed to stroke outcome.

Details

Language :
English
ISSN :
1872-8421
Volume :
212
Issue :
1-2
Database :
MEDLINE
Journal :
Journal of neuroimmunology
Publication Type :
Academic Journal
Accession number :
19457561
Full Text :
https://doi.org/10.1016/j.jneuroim.2009.04.007