کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
3257279 | 1207403 | 2011 | 10 صفحه PDF | دانلود رایگان |
In this study we explored the effects of galectin-9 on CVB3 induced myocarditis and its possible mechanisms involved. We demonstrated that galectin-9 expression was significantly up-regulated in the myocardium following CVB3 infection and was correlated with the severity of viral myocarditis. To explore whether galectin-9 may have therapeutic effect on the CVB3 induced myocarditis, galectin-9 was administered daily to mice following CVB3 infection. Significantly reduced CD4+ T cells and remarkably increased regulatory T cells frequency in the heart tissue were found as compared to the non-treated mice. It was accompanied by a significant decreased level of Th1 cytokines as TNF-α and IFN-γ both in the myocardium and serum, and an increased level of Th2 cytokines such as IL-4 and IL-10. Galectin-9 was further found to promote the proliferation of regulatory T cells and elevated IL-4-secreting Th2 cells. It may represent as a novel therapeutic strategy in treating Th1-mediated inflammatory cardiac disease.
► Up-regulation of Gal-9 was closely associated with CVB3 induced myocarditis.
► Gal-9 treatment had a therapeutic effect on the CVB3-myocarditis.
► Gal-9 administration selectively up-regulated anti-inflammatory Th2 and Treg population in the heart tissue.
► Gal-9 administration significantly decreased the pro-inflammatory Th1 cytokines while elevated Th2 cytokines production in the myocardiac tissue.
Journal: Clinical Immunology - Volume 140, Issue 1, July 2011, Pages 92–101