Abstract
Human neutrophils constitutively undergo apoptosis, process which is critical for the successful resolution of inflammation by the safe removal of effete cells. A wide variety of agents can modulate neutrophil apoptosis and these act through multiple and complex receptor-signalling pathways. Whilst these pathways can be initiated via distinct cell surface receptors, many downstream intracellular pathways can converge, use common molecules or trigger similar cellular activities, such as activation of caspases and transcription factors. The cell surface receptors, TNFR and Fas both trigger apoptosis in certain cell types, including neutrophils. However, TNF receptors also activate survival mechanisms in human neutrophils. This review summarises current knowledge about the regulation of neutrophil apoptosis via death receptors, the molecular components involved in signalling and potential therapeutic targets that are based on death receptors or their signalling pathways.