Characterization of Fc receptors for IgE on human alveolar macrophages.

Human alveolar macrophages (aM phi) isolated from lung lavages performed during bronchoscopy and after surgical removal of pulmonary lobes were analysed for Fc receptors for IgE (Fc epsilon R) and IgG (Fc gamma R) by rosette assays. A mean+/-s.d. of 8.0+/-2.6% of aM phi formed rosettes with fixed ox erythrocytes coated with an IgE myeloma protein (Eo'-IgE). The Eo'-IgE rosettes were inhibited by two IgE myeloma proteins and by IgE Fc fragments but not by myeloma proteins of the other Ig classes or by IgE denatured by heating or reduction and alkylation. Fresh ox erythrocytes sensitized with rabbit IgG antibodies (EoA) formed rosettes with 64.1+/-20.3% of the aM phi. Peripheral blood monocytes formed 10.6+/-1.2% Eo'-IgE and 90.2+/-6.0% EoA rosettes. Incubation of the aM phi with a goat antiserum to human lymphocyte Fc epsilon R inhibited Eo'-IgE rosette formation on aM phi by 80% but did not affect the percentage of EoA rosettes. The antiserum also inhibited Eo'-IgE rosettes formed by peripheral blood monocytes and cultured macrophage-like U937 cells but not those formed by basophilic granulocytes obtained from a patient with chronic myelogenous leukaemia. There was no relationship between age, sex, diagnosis or smoking history of the patients and the percentage of aM phi forming Eo'-IgE rosettes. These studies demonstrate that a subpopulation of human aM phi bear Fc epsilon R that share antigenic determinants with Fc epsilon R on lymphocytes and monocytes. Fc epsilon R(+) aM phi may play an important role in allergic and inflammatory pulmonary diseases by inducing the release of mediators of inflammation after interaction with IgE immune complexes.