Viral myocarditis in adult C57BL/6 mice results is a self-limiting and mild disease but results in persistent cardiac pathology as demonstrated by permanent myocardium scarring and left ventricle (LV) dysfunction. We have characterized the cells involved in the immune responses within the heart during viral myocarditis. The first and most abundant cells to infiltrate the heart are monocytes and monocyte-derived MFs (Ly6C+), and in much smaller number neutrophils. In contrast to other innate cells, DCs are reduced in the heart 4 days after infection, moment at which we could observe the inception of the T cell response in the draining LN (using newly a developed EMCV-D-specific MHC-I tetramer), suggesting a migration of cardiac DCs towards the draining LNs to initiate the T cell response. Identification of activated T cells did not occur in the myocardium until days 6-7 post-infection, coinciding with the waning of viral burden. In addition, our data infecting T- and B-cell deficient mice (Rag1-/-) that adaptive and innate immune responses are essential for the prevention of deathly infection.
An important line of research in my lab consists on studying how immune cell responses determine viral myocarditis outcomes in adult and neonatal individuals.