SOCS1 DNA administration protected mice from the development of experimental autoimmune myocarditis and heart failure by reducing the activation of autoreactive CD4(+) T cells.
Does SOCS1 DNA administration prevent the development of experimental autoimmune myocarditis and heart failure in mice?
SOCS1 DNA administration protects against experimental autoimmune myocarditis and heart failure in mice by inhibiting autoreactive T cell activation, suggesting therapeutic potential for autoimmune myocarditis.
Myocarditis and subsequent dilated cardiomyopathy are major causes of heart failure in young adults. Myocarditis in humans is highly heterogeneous in etiology. Recent studies have indicated that a subgroup of myocarditis patients may benefit from immune-targeted therapies, because autoimmunity plays an important role in myocarditis as well as contributing to the progression to cardiomyopathy and heart failure. Suppressor of cytokine signaling (SOCS) 1 plays a key role in the negative regulation of both TLR- and cytokine receptor-mediated signaling, which is involved in innate immunity and subsequent adaptive immunity. In this study, we investigated the therapeutic effect of SOCS1 DNA administration on experimental autoimmune myocarditis (EAM) in mice. EAM was induced by s.c. immunization with cardiac-specific peptides derived from α myosin H chain in BALB/c mice. In contrast to control myocarditis mice, SOCS1 DNA-injected mice were protected from development of EAM and heart failure. SOCS1 DNA administration was effective for reducing the activation of autoreactive CD4(+) T cells by inhibition of the function of Ag-presenting dendritic cells. Our findings suggest that SOCS1 DNA administration has considerable therapeutic potential in individuals with autoimmune myocarditis and dilated cardiomyopathy.
Tajiri et al. (2012) studied Experimental autoimmune myocarditis. SOCS1 DNA vs. Control myocarditis mice was evaluated on Development of experimental autoimmune myocarditis and heart failure. SOCS1 DNA administration protected mice from the development of experimental autoimmune myocarditis and heart failure by reducing the activation of autoreactive CD4(+) T cells.