(A) Dot plots depict flow cytometric analysis of macrophage/monocyte populations in B6 CD45.2⁺ heart grafts 2 hours after transplantation into congenic B6 CD45.1⁺ hosts. CCR2^–MHCII^hi, CCR2^–MHCII^lo, and CCR2⁺MHCII^hi macrophages and CCR2⁺MHCII^lo monocytes are present. Macrophage/monocyte populations are gated on donor hematopoietic (CD45.2⁺CD45.1^–) and myeloid (CD11b⁺CD64⁺) cells. Plots are representative of 4 independent experiments with comparable results. (B) Quantification of donor monocyte/macrophage populations represented as percentage of CD45.2⁺CD11b⁺CD64⁺ cells based on gating depicted in A. Neutrophil (green) trafficking in (C) control diphtheria toxin–treated (DT-treated) WT (see Supplemental Video 3; n = 4 mice)or (D) DT-treated CCR2-DTR (DT receptor) heart grafts (see Supplemental Video 4; n = 5 mice). Blood vessels appear red after injection of quantum dots (n = 4 mice). (E) Percentage of neutrophils that extravasated during imaging period was significantly higher in hearts derived from DT-treated WT donors compared with heart grafts harvested from DT-treated CCR2-DTR mice. (F) Neutrophil rolling velocities were comparable in coronary veins of cardiac grafts derived from DT-treated WT and DT-treated CCR2-DTR mice. (G) Intraluminal crawling velocities were significantly lower in hearts harvested from DT-treated CCR2-DTR compared with DT-treated WT mice. **P < 0.01 (t test). Data in E, F, and G are derived from 4 mice receiving hearts from DT-treated WT mice and 5 recipients of cardiac grafts derived from DT-treated CCR2-DTR donors. For F and G, symbols represent averages obtained from individual mice with over 30 neutrophils examined per mouse, horizontal bars denote means, and error bars denote ±SEM.