In addition to monocytes, neutrophils are rapidly recruited over the first 24 hours after MI to the site of injury and start degrading extracellular matrix components as well as phagocytising dead cells. According to several surface markers it is possible to distinguish between resident and inflammatory macrophages and to describe a two phasic monocyte/macrophage VE-822 response after MI. The first phase is mainly affected by Ly6Chigh, inflammatory monocytes/macrophages, while the second phase is dominated by the accumulation of Ly6Clow, tissue repairing monocytes/macrophages. Current findings of Epelman et al. highlight that the immune system in the heart is uniquely adapted to the demands of physiological and pathological stress in steady state and after injury. However, the dynamics of the immune response in the context of chronic pressure overload and consecutive LV tissue remodeling are incompletely understood. Our group recently verified the impact of MAC2+ cells in the development of cardiac hypertrophy but has not yet characterized the distinct macrophage subpopulations according to their surface expression of F4/80 and Ly6C following the definition of Geissman et al.. Recently using a murine model of urinary tract infection we found that F4/80+, Ly6Chigh phagocytes showed pro-inflammatory helper macrophage functions by secreting TNF, while F4/80+, Ly6Clow phagocytes acted as sentinel macrophages and displayed helper-cell functions by secreting CXCL2, allowing neutrophil transepithelial migration. The process of recruitment and activation of innate and adaptive immune cells could provide the initial point for immune modulatory strategies to ameliorate LV remodelling and cardiac function. Recent studies highlight that uncontrolled, overshooting monocyte response can impair scar formation after myocardial infarction. Recruitment of monocytes and neutrophils from the circulatory system are important for the induction and maintenance of inflammatory processes. After myocardial infarction, recruited monocytes and macrophages play a critical role in cardiac tissue remodeling. The migration of myeloid cells is controlled by specific chemoattractants, called chemokines, and the expression of adhesion molecules on the surface of immune cells and endothelial cells. Here, the expression of the integrin heterodimer CD11b, also known as Mac-1, on the surface of monocytes and granulocytes directly influences cell adhesion and transendothelial migration as it interacts with the intercellular adhesion molecule 1 on endothelial cells. Moreover, platelet/ endothelial-cell adhesion molecule 1, also known as CD31 has been reported to be another important junctional molecule, for which leukocytes express ligands, that facilitates cell adhesion and extravasation. In that context, the chemokine receptor CX3CR1, which is also known as fractalkine receptor, contributes to cell recruitment during inflammation through chemotaxis and mediation of adhesion. Moreover, CX3CR1 can be used to distinguish between different monocyte/macrophage populations, as Ly6Clow monocytes/macrophages express more CX3CR1 than Ly6Chigh cells. In addition, CX3CR1 is required for monocyte crawling or patrolling in the lumen of the blood vessels.