Myocardits is an inflammation of the heart muscles that is a major cause of heart failure in young patients. In some cases, the disease is caused by viral infection, but in other patients it is linked to an autoimmune attack on the heart muscle. There are few effective treatment options for myocarditis, in part because the molecular mechanisms that underlie the defect are poorly defined.
In this paper, researchers led by Myra Lipes, at the Joslin Diabetes Center in Boston, Massachusetts, used a mouse model of spontaneous myocarditis. They found that the disease occurs because the immune system recognizes a protein required for the heart muscle to contract called alpha myosin as a pathogenic molecule, and T cells begin attacking the muscle cells that express it. However, they also demonstrated that they could prevent the disease from occurring in mice if the T cells were exposed to alpha myosin in the thymus as they developed. In the accompanying commentary, Todd Metzger and Mark Anderson at the University of California, San Francisco, suggest that although additional clinical research will be critical, the findings in this paper suggest that measurement of α-myosin might be a useful diagnostic tool for myocarditis, and further that the protein could be a promising therapeutic target.