FcγRIIA/CD32A expression severely aggravates the alveolar edema and increases the mortality of antibody-mediated TRALI. The pathogenesis of TRALI was analyzed 15 minutes or 2 hours after injection of the chimeric human/mouse anti–MHC I mAb hIgG1-34-1-2S (1.5 mg/kg, intravenous) into LPS-sensitized (0.1 mg/kg, intraperitoneal) CD32A^– or CD32A⁺ mice. (A) Protein concentrations in BALs were measured 15 minutes after injection of hIgG1-34-1-2S or in negative controls (CD32A^–, n = 9-20; CD32A⁺, n = 3-20). (B) The histologic features of lung injury were determined 15 minutes after injection of hIgG1-34-1-2S or in negative controls (CD32A^–, n = 7-17; CD32A⁺, n = 7-19). Scale bar = 200 µm. (C) Exemplary photographs showing increased pulmonary vascular permeability in CD32A⁺ mice compared with CD32A^– mice revealed by extravasation of Evans Blue dye into the lung tissue and BALs 15 minutes after administration of hIgG1-34-1-2S. (D) Extravasation of Evans Blue dye was not observed in the vascular territories of the glabrous skin of the ears, snout, or paws 15 minutes after injection of hIgG1-34-1-2S or saline into CD32A⁺ or CD32A^– mice. (E) Left: Kaplan-Meier survival plots for CD32A^– and CD32A⁺ mice (n = 10) (log-rank test, P = .0027). Right: Protein concentrations in BALs of CD32A^– and CD32A⁺ mice at death or at the 2-hour end point. Results are presented as the mean ± standard error of the mean. *P < .05, **P < .01, ***P < .001 by one-way analysis of variance (panels A and B) or a Student t test (panel E, right).