期刊
JOURNAL OF IMMUNOLOGY
卷 186, 期 4, 页码 2561-2570出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1002029
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资金
- Deutsche Forschungsgesellschaft [TR-SFB 19, Z3]
- Deutsche Stiftung fur Herzforschung of the Deutsche Herzstiftung [F 01/10]
TRIF is a member of the innate immune system known to be involved in viral recognition and type I IFN activation. Because IFNs are thought to play an important role in viral myocarditis, we investigated the role of TRIF in induced myocarditis in mice. Whereas C57BL/6 (wild-type) mice showed only mild myocarditis, including normal survival postinfection with coxsackievirus group B serotype 3 (CVB3), infection of TRIF(-/-) mice led to the induction of cardiac remodeling, severe heart failure, and 100% mortality (p < 0.0001). These mice showed markedly reduced virus control in cardiac tissues and cardiomyocytes. This was accompained with dynamic cardiac cytokine activation in the heart, including a suppression of the antiviral cytokine IFN-beta in the early viremic phase. TRIF(-/-) myocytes displayed a TLR4-dependent suppression of IFN-beta, and pharmacological treatment of CVB3-infected TRIF(-/-) mice with murine IFN-beta led to improved virus control and reduced cardiac inflammation. Additionally, this treatment within the viremic phase of myocarditis showed a significant long-term outcome indexed by reduced mortality (20 versus 100%; p < 0.001). TRIF is essential toward a cardioprotection against CVB3 infection. The Journal of Immunology, 2011, 186: 2561-2570.
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