**5. Concluding remarks**

Beside direct effects of replicating viruses, unbalanced autoimmune responses associated with the production of auto-antibodies against cardiac tissue may also contribute to the progression of myocardial injury in inflammatory heart disease (Eriksson et al., 2003). The detection of auto-reactive antibodies directed against a number of different cardiac antigens is a prominent feature of all forms of persistent myocarditis and inflammatory cardiomyopathy, and there are reports demonstrating that the presence of anti-myosin autoantibodies is associated with deterioration of left ventricular function (Liu and Mason, 2001; Shishido et al., 2003; Dörner et al., 2005; Rose, 2009). In addition to the critical role of TLRs in mediating cardiac dysfunction in infectious conditions, emerging evidence suggests that the TLRs are also involved in modulating cardiomyocyte survival and ischemic myocardial injury (Chao, 2009; Riad et al., 2008). Despite significant progress in the identification of receptors triggering innate immune responses, further research is necessary to unravel the cooperative interactions between the innate and acquired immune system active in the protection of the heart against viral or autoimmune damage.
