To confirm that the increased IL-4 and decreased IFN-γ levels that we had observed in the heart of TLR3-deficient mice during acute myocarditis were due to a shift to a classic Th2 response, we examined markers of IL-4-driven alternative activation in the heart by qRT-PCR (Figure 7) [23, 24]. This evidence concerns the gene IFNG and myocarditis.