Mechanism of delayed CGD neutrophil apoptosis. CGD neutrophils undergo normal rolling and adhesion onto activated endothelium. The neutrophils then undergo diapedesis in response to chemotactic stimuli into tissue. The neutrophils are able to ingest bacteria but manifest impaired apoptosis accompanied by prolonged release of proteases into tissue from primary granules, thereby generating sterile inflammation. The CGD macrophage fails to ingest the CGD neutrophil because of reduced exposure of phosphatidylserine (PS) on the neutrophil membrane. In turn, the failure to express normal amounts of PS leads to failure to activate phosphatidylserine receptors (PSRs) on the CGD macrophage, leading to attenuated production of endogenous IL-4, a required cytokine necessary to initiate stimulus-response coupling required for macrophage activation. Professional illustration by Paulette Dennis.