Editorial

In mammals, billions of cells are turned over daily in a continuous succession of cell death and replacement. This occurs as part of either routine homeostasis (aged or excess cells) or after acute injury. These cells die usually by the pro-cess of apoptosis and are rapidly removed by neighboring or recruited phagocytes.1 Unlike phagocytosis of pathogens, apoptotic cell clearance actively induces immunosuppressive signaling.2 Few apoptotic cells can usually be detected, even in the tissues with high cellular turnover, because of the quick removal by phagocytes.3 The clearance of apoptotic cells criti-cally depends on the function of phagocyte engulfment recep-tors, which recognize the apoptotic cell eat-me signals and mediate their removal.4 Defects in engulfment are linked to the development of autoimmunity in mice and humans, pre-sumably because of the secondary necrosis of the dying cells and the release of their cellular contents, which activate th