The last few years have seen the accumulation of compelling evidence that apoptosis (programmed cell death) plays a major role in promoting resolution of the acute inflammatory response. Neutrophils are constitutively programmed to undergo apoptosis, which limits their pro-inflammatory potential and leads to rapid, specific, and non-phlogistic recognition by macrophages and semi-professional phagocytes. Similar mechanisms have been implicated in clearance of eosinophils, lymphocytes, and monocytes and apoptosis also plays a role in remodeling the inflamed site by deletion of myofibroblasts. A growing understanding of the mechanisms regulating leukocyte apoptosis and of the molecules mediating safe phagocytic clearance of dying cells may yield new insights into the pathogenesis and therapy of inflammatory diseases.