Colony-stimulating factors (CSFs) have important effects on mature myeloid cells in addition to their regulatory role in haemopoiesis. Exposure of neutrophils to granulocyte macrophage-CSF (GM-CSF) increases chemotaxis, phagocytosis and cytotoxicity and primes the cells for enhanced oxidative metabolism in response to stimuli, such as formylated oligopeptides derived from bacteria (f-Met-Leu-Phe) and endogenous activated complement components (C5a). GM-CSF induces time-dependent changes in neutrophil f-Met-Leu-Phe receptor number and affinity that correspond to changes in functional activity. The neutrophil IgA Fc receptor is also modulated by GM-CSF such that it develops a high affinity state and transduces a phagocytic signal. The ability to regulate the number and activity of mature myeloid effector cells in vivo establishes unique therapeutic opportunities in the area of infectious disease, cancer treatment, bone marrow transplantation and augmentation of host defence in immunodeficient patients.