Neutrophils and macrophages work in concert as inducers and effectors of adaptive immunity against extracellular and intracellular microbial pathogens.

Emerging data suggest new facets of the concerted participation of neutrophils and macrophages in antimicrobial immunity. The classical view is that DCs and macrophages are the inducers of adaptive antimicrobial immunity, but there is evidence for neutrophil participation in this task as cytokine and chemokine producers and APCs. On the other hand, the concept that the T(H)1 response is only associated with control of infections by intracellular pathogens through activation of macrophages by IFN-gamma, and the T(H)17/IL-17 axis is only involved in protection against extracellular pathogens through mobilization and activation of neutrophils is simplistic: There is evidence suggesting that T(H)1 and T(H)17 responses, separately or in parallel, may use macrophages and neutrophils against infections by extracellular and intracellular microbial pathogens. Opsonization by pathogen-specific Igs enhances the antimicrobial capabilities of neutrophils and macrophages in infections by extracellular and intracellular microbes. The functional partnership between macrophages and neutrophils as inducers and effectors of adaptive antimicrobial immunity conforms to their affiliation with the myeloid phagocyte system and reveals a strategy based on the concurrent use of the two professional phagocytes in the adaptive defense mechanisms. Starting from a common myeloid precursor in the bone marrow, macrophages and neutrophils split during differentiation but come together at the infectious foci for a cooperative strategy that uses modulator and effector activities to attack invading microbial pathogens.