Chronic inflammation after a heart attack can promote heart failure and death. The 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.
The current research evolved out of an impactful 2013 paper that was named one of the five most outstanding papers in Circulation Research for the year. In Remodeling of the Mononuclear Phagocyte Network Underlies Chronic Inflammation and Disease Progression in Heart Failure: Critical Importance of the Cardiosplenic Axis, Prabhu and colleagues showed that immune cells that are stored in the spleen were intricately involved in the heart failure that follows a heart attack, or infarction, in a mouse model system. The splenic immune cells that invaded the heart tissue included pro-inflammatory macrophages and dendritic cells.
Since a primary function of the dendritic cells is to present an antigen to T-cells, to activate the T-cells and begin the immune response, the researchers suspected that T-cell activation in the heart tissue, and perhaps heart tissue injury caused by T-cells, might be central to the pathological heart enlargement that is called remodeling.