Evidence that C1q,a Subcomponent of the First Component of Complement,is an Fc Receptor of Peritoneal and Alveolar Macrophages

Guinea pig peritoneal macrophages were cultured for 24 h in the presence of two inhibitors of the biosynthesis of collagen-like molecules such as C1q : 10^-3 M 3,4-dehydroproline or 10^-4 M 2,2′-dipyridyl. Their Fc-receptor activity was measured by rosette formation, using sheep erythrocytes (E) coated with rabbit anti-sheep IgG (EA_IgG). The Fc-receptor activity was decreased by 40 to 70% of control cultures depending on the amount of IgG on the E. The activity of a second receptor on the macrophages, mediating the binding of C3b coated E, was not altered by this treatment.Rat alveolar macrophages were depleted of their Fc-receptor activity by pronase treatment (1.5 mg/ml) in the presence of 2,2′-dipyridyl. After washing the cells, the EA_IgG-binding activity was restored to about half of the initial level within 2 h. With 2,2′-dipyridyl also present during the second incubation, the re-expression of the Fc-receptor activity was suppressed further.Preincubation of guinea pig peritoneal macrophages with anti-C1q-F(ab')₂ for 45 min at 37°C caused a dose-dependent reduction of the Fc-receptor activity, but not C3b receptor activity.These results support our hypothesis that C1q synthesized and secreted by macrophages serves as an Fc-receptor in the membrane during the secretion.