FcγRIIA can induce acute airway inflammation. (A-B) Sections of (A) human lung or (B) lung from 3KO or 3KOIIA mice, stained with Hematoxilin (blue) and anti-FcγRIIA rabbit antiserum (red). (C) Representative expression of FcγRIIA on mouse alveolar macrophages (CD11c+/Gr1−) from 3KOIIA (open histogram) and 3KO (filled histogram) mice. (D) F(ab′)2 DAR-FITC staining of WT or FcγRIIA-expressing CHO transfectants incubated with preformed ICs made of OVA and rabbit anti-OVA antiserum (open histograms) or not (filled histograms). (E-F) Representative density plots of CD45+ BAL cells from indicated mice (E) left untreated or (F) injected with antigen intravenously and antiserum intranasally. Cell types were discriminated as alveolar macrophages (CD11c+/Gr1int, oval gate) and neutrophils (CD11c−/Gr1hi, rectangular gate). (G-J) Time course of (G) cell counts, (H) MPO level, (I) hemorrhage score, and (J) KC levels in BAL from indicated mice after injection with antigen intravenously and antiserum intranasally (n ≥ 3). (K) KC secretion or (L) MIP-1α secretion by purified alveolar macrophages from indicated mice incubated ex vivo on plate-bound rabbit IgG-ICs (OVA–anti-OVA) or IV.3 mAb. (G-L) Data are represented as mean ± SEM. (A-L) Data are representative from at least 2 independent experiments, and (J) data are a compilation of 2 experiments (*P < .05; **P < .01; ***P < .001).