Fig. 1

Neutrophil fates under homeostatic or inflammatory conditions. Neutrophils arise from precursor cells in the bone marrow and are released into the bloodstream, from where they set out to patrol the internal tissues as well as the ocular surfaces and exocrine ducts. Under homeostatic conditions (green box), neutrophils undergo different fates: (a) NET formation and excretion, (b) in situ apoptosis or (c) re-circulation to the bone marrow and clearance. Under inflammatory conditions (red box), neutrophils are attracted to the site of infection or damage (d) first through a sequential combination of long- and short-ranging chemoattractants. The latter mediates the coordinated extravascular aggregation dynamics known as swarming behavior. Kienle et al.¹ now show that preprogrammed desensitization of the very G-protein-coupled receptors (GPCRs) that drive swarming is an intrinsic feedback control that leads to dynamic arrest (e). This arrest ensures stable cluster formation and is critical for their antibacterial effector functions. Successful elimination of the invading pathogen is then followed by apoptosis in situ and elimination by recruited phagocytes (f), which is the trigger for the active resolution of inflammation