Chronic inflammation after a heart attack can promote heart failure and death. University of Alabama at Birmingham researchers have now shown that activated T–cells – part of the immune system’s inflammatory response – are both necessary and sufficient to produce such heart failure. “These studies,” Shyam Bansal, PhD, Sumanth Prabhu, MD, and colleagues write in the journal Circulation: Heart Failure, “provide important proof–of–concept for T–cells as disease mediators in heart failure.”

Two key experiments demonstrated this necessary and sufficient role for the activated T–cells, which presumably attack heart muscle tissue in an auto–immune fashion.

The first key experiment involved removing a specific subset of activated T–cells from mouse models. Treating the mice with antibodies against CD4+ T–cells four weeks after experimental heart attacks – to deplete that subset of T–cells – prevented the progressive abnormal enlargement of the left ventricle that leads to heart failure, as compared with untreated mice.

The second key experiment showed the effect of transferring activated T–cells from heart–attack mice to healthy mice. When spleen CD4+ T–cells were transferred from heart–attack donor mice to naïve recipient mice, they induced long–term left ventricle dysfunction, fibrosis and enlargement, hallmarks of heart failure.

These findings could translate to the clinic, the researchers say. “Our data suggests that targeting specific immune cell subsets at defined stages of disease may represent a better approach to therapeutic immunomodulation to improve heart failure.