Mechanisms and strategies for a therapeutic cardiac immune response

Abstract

Even healthy, homeostatic myocardium is populated by a variety of immune cells - most prominently resident macrophages, dendritic cells, patrolling monocytes, mast cells, B cells, and T cells [1–3] (Fig. 1A). Virtually every form of cardiac stress can alter immune cell composition and phenotype, for example by polarizing macrophages into pro-inflammatory or immunomodulatory states [4], promoting T cell maturation into effector or regulatory phenotypes [5], or inducing neutrophil infiltration [6].