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Summary
Neutrophils and monocyte-derived macrophages are myeloid cells, with a shared hematopoietic ancestry, that pursue both common and distinct immune functions. In response to tissue damage or infection, neutrophils infiltrate first, followed by monocytes (1). Through a series of events involving the release of proinflammatory products, both cell types seek to neutralize danger, and if successful, inflammation resolves. But when stimuli persist and inflammation is not resolved, neutrophils and monocytes continue to accumulate, presumably inflicting the irreversible damage that characterizes chronic inflammation. Whether neutrophils and monocytes act together to fuel the inflammatory cascade in those circumstances is still poorly understood. On page 316 of this issue, Warnatsch et al. (2) report that neutrophils prime macrophages for inflammatory responses that aggravate atherosclerosis. Neutrophil extracellular traps (NETs) underlie the communication between these two immune cell types.
