Also, in a mouse model of MI, depletion of resident CCR2+ macrophages resulted in substantially less monocyte, macrophage, and neutrophil recruitment in the first 2 days following myocardial injury, and reduced interstitial fibrosis after 28 days, suggesting that depletion of CCR2+ macrophages alone is enough to limit the initial inflammatory response and subsequent fibrosis. Here, CCR2 is linked to myocardial infarction.