Inflammation plays a crucial role in cardiac repair, but may also extend ischemic injury and contribute to post-infarction remodeling. This review manuscript discusses recent advances in our understanding of the cell biology of the post-infarction inflammatory response. Recently published studies demonstrated that the functional repertoire of inflammatory and reparative cells may extend beyond the roles suggested by traditional teachings. Neutrophils may play an important role in cardiac repair by driving macrophages toward a reparative phenotype. Subsets of activated fibroblasts have been implicated in protection of ischemic cardiomyocytes, in phagocytosis of apoptotic cells, and in regulation of inflammation. Dissection of the cellular effectors of cardiac repair is critical in order to develop new therapeutic strategies for patients with acute myocardial infarction.