Recent studies have suggested that macrophages in steady-state tissues originate from embryonic yolk sac-derived progenitors and are maintained by self-renewal in situ. Bain et al. now report that this paradigm does not hold true for intestinal macrophages. They have found that embryonic precursor cells seed the intestinal mucosa and show extensive proliferation during the neonatal period. However, these cells are replaced around the time of weaning by LY6Chi monocytes, which are recruited to the intestine in a CC-chemokine receptor 2 (CCR2)-dependent manner and mature into anti-inflammatory macrophages. Recruitment of monocytes to the intestine required signals from the microbiota and was responsible for maintaining intestinal macrophage populations throughout adulthood. The authors suggest that this unique mode of replenishing macrophages may reflect the continuous threat of infection and tissue damage in the intestine.