Figure 1.

Summary characteristics of immune cells involved in development and resolution of inflammation post-myocardial infarction. Cells of the immune system may input either successful or unsuccessful myocardial remodeling after myocardial infarction, being involved in all the three phases of cardiac repair: inflammatory phase; reparative and proliferative phase; maturation phase. Some cellular populations (monocytes, macrophages, lymphocytes) are represented by two or more subsets with opposite or complementary effects. At the same time, some immune cells may exhibit either inflammatory or reparative properties, depending on the nature of the signal and cellular milieu (eosinophils, dendritic cells, mast cells, NK cells, iNKT cells). Possibility exists that new distinct subpopulations of immune cells are yet to be described, and inflammatory and reparative functions will further be ascribed to different cellular subsets. CCL CC, Chemokine ligand; CD, Cluster of differentiation; ECP, Eosinophil cationic protein; FGF, Fibroblast growth factor; IFN, Interferon; Ig, Immunoglobulin; IL, Interleukin; IL-1Ra, Interleukin-1 receptor antagonist; MBP, Major basic protein; MMP, Matrix metalloproteinase; MPO, Myeloperoxidase; NO, Nitric oxide; ROS, Reactive oxygen species; TGF, Transforming growth factor; TNF, Tumor necrosis factor; VEGF, Vascular endothelial growth factor; Question marks indicate absent or incomplete data and facts that have not been sufficiently studied for myocardial infarction.