Recent studies of heart disease suggest that immunologically mediated
processes often accompany cardiac injury and can contribute to pathoge
nesis. Murine models of myocarditis have provided insight into the mec
hanisms by which autoimmune responses to cardiac antigens arise and ca
use tissue pathology, It is now evident that T cells, cytokines and an
tibodies can all contribute to cardiac injury. Furthermore, murine mod
els have demonstrated that both the propensity to develop autoreactivi
ty following cardiac injury and the vulnerability of the heart to thes
e responses are under genetic control. Continued studies will help to
identify susceptibility genes and might aid in the development of stra
tegies to protect individuals at risk from immunologically mediated da
mage following cardiac injury.