Circulation Journal
Online ISSN : 1347-4820
Print ISSN : 1346-9843
ISSN-L : 1346-9843
Experimental Investigation
Alteration of IL-17 Related Protein Expressions in Experimental Autoimmune Myocarditis and Inhibition of IL-17 by IL-10-Ig Fusion Gene Transfer
He Chang, Haruo Hanawa, Tsuyoshi Yoshida, Manabu Hayashi, Hui Liu, Limin Ding, Keita Otaki, Kazuhisa Hao, Kaori Yoshida, Kiminori Kato, Ken Toba, Makoto Kodama, Hiroki Maruyama, Junichi Miyazaki, Yoshifusa Aizawa
Author information
Keywords: Cardiomyopathy, Gene therapy, Interleukin-17, Th17, Th1/Th2 balance
JOURNAL FREE ACCESS

2008 Volume 72 Issue 5 Pages 813-819

Details
Download PDF (148K)
Download citation RIS

(compatible with EndNote, Reference Manager, ProCite, RefWorks)

BIB TEX

(compatible with BibDesk, LaTeX)

Text
How to download citation
Contact us
Abstract

Background T-helper (Th)1/Th2 cytokine balance plays an important role in the pathogenesis of myocarditis. Recently, some studies indicate that interleukin (IL)-17, known as a T cell (Th17)-derived proinflammatory cytokine, is the major mediator of tissue inflammation in inflammatory and autoimmune diseases. Experimental autoimmune myocarditis (EAM) is a T cell-mediated autoimmune disease; however, the pathogenic role of IL-17 in the development of rat EAM remains largely unknown. Methods and Results In the present study, alterations of IL-17-related protein expressions were investigated and then the effect of hydrodynamic-based delivery of plasmid DNA encoding the IL-10-Ig gene on rat EAM and the effect of IL-10-Ig on IL-17 was evaluated. The results showed that IL-17 was expressed more highly than IFN-γ expressed by Th1 cells in αβT cells and the peaks of IL-17 related protein expression in the heart were the early phase of EAM. Moreover, we observed that IL-10-Ig gene therapy was effective in controlling EAM and that IL-10-Ig significantly suppressed the expression of IL-17 as well as other proinflammatory cytokines, IL-1β and TNF-α, in IL-1-stimulated splenocytes cultured from EAM rats. Conclusions IL-17 is highly produced by αβT cells in the early phase of EAM hearts and IL-17 inhibition might be a possible mechanism of the amelioration of EAM by IL-10-Ig treatment. These data suggest that IL-17 produced by Th17 plays an important role in the pathogenesis of rat EAM. (Circ J 2008; 72: 813 - 819)

Content from these authors
© 2008 THE JAPANESE CIRCULATION SOCIETY
Previous article Next article
Favorites & Alerts

Recently viewed articles
Predecessor

The Nippon Journal of Clinical Angio-Cardiology

Japanese Circulation Journal

JAPANESE CIRCULATION JOURNAL

Related information

Request a Permission

Related journals
Circulation Reports
Share this page
feedback
 Top