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mental component of the innate immune system, forming an efficient barrier against invading microbial pathogens. Neutropenia, a common unwanted side effect of chemotherapy, is associated with infectious complications. The human bone marrow produces an estimated number of 1011 neutrophils per day, and granulopoi-esis physiologically takes up two-thirds of the hematopoietic marrow space. The regulation of neutrophil numbers in the steady state remains incompletely understood. More recent evidence, how-ever, suggests that it depends on separate hematopoietic signaling pathways as com-pared with “emergency granulopoiesis,” elicited by injection of infectious agents into experimental mice.1 A “neutrostat” has been suggested to detect neutro-phils released by the marrow (“turnstile” hypothesis) or, alternatively, to measure the number of apoptotic neutrophils phagocytosed by tissue macrophages.2 Indeed, adhesion molecule-deficient mice, whose neutrophils are unable to transmigrate, display pronounced neutro-philia. The underlying mechanism was elegantly shown to represent disinhib-ited macrophage-derived IL-23 secretion, which, in turn, stimulates T