| First Author | Riad A | Year | 2011 |
| Journal | J Immunol | Volume | 186 |
| Issue | 4 | Pages | 2561-70 |
| PubMed ID | 21239721 | Mgi Jnum | J:169158 |
| Mgi Id | MGI:4939959 | Doi | 10.4049/jimmunol.1002029 |
| Citation | Riad A, et al. (2011) TRIF is a critical survival factor in viral cardiomyopathy. J Immunol 186(4):2561-70 |
| abstractText | 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. |
