Cells undergoing programmed cell death (apoptosis) are cleared rapidly in vivo by phagocytes without inducing inflammation(1), Here we show that the glycosylphosphatidylinositol-linked plasma-membrane glycoprotein CD14 (refs 2, 3) on the surface of human macrophages is important for the recognition and clearance of apoptotic cells, CD14 can also act as a receptor that binds bacterial lipopolysaccharide (LPS), triggering inflammatory responses(4), Overstimulation of CD14 by LPS can cause the often fatal toxic-shock syndrome(5,6). Here we show that apoptotic cells interact with CD14, triggering phagocytosis of the apoptotic cells, This interaction depends on a region of CD14 that is identical to, or at least closely associated with, a region known to bind LPS, However, apoptotic cells, unlike LPS, do not provoke the release of pro-inflammatory cytokines from macrophages, These results indicate that clearance of apoptotic cells is mediated by a receptor whose interactions with ＇non-self＇ components (LPS) and ＇self＇ components (apoptotic cells) produce distinct macrophage responses.