The remodeling and reparative process post myocardial infarction (MI) can be divided into three phases: the inflammatory phase, the proliferative phase and the stable phase. The inflammatory immune response plays an important part in the process of cardiac remodeling. First of all, the initiation of inflammatory response relies on the activation of innate immunity with a group of pro-inflammatory cytokines, chemokines and adhesion molecules. These molecules lead to the infiltration of the infarct area with neutrophils and mononuclear cells, further clearing the wound from dead cardiomyocytes and matrix debris. After resolution of inflammatory response, reparative cells and cytokines infiltrate into the heart and promote the differentiation and growth of myofibroblasts and endothelial cells, contributing to wound contraction as well as producing fiber tissue to form a scar. Moreover, overactive immune responses could accentuate infarct injury and dilative remodeling while deficiency of inflammation leads to insufficient repair, which highlights the dual function of the immune response in myocardial injury and repair post MI. Also the intense immune response along with fibrosis in non-infarct area is also closely associated with adverse remodeling. Thus, targeting specific factors in the inflammatory reaction may hold promise in patients with MI.