Systemic administration of CD16A-Ig efficiently blocked the reversed passive Arthus reaction in vivo in mice without complement depletion. (A) The mice (n = 3) were injected with various concentrations of CD16A-Ig intravenously (panel iv, 5 μg/mL; panel v, 25 μg/mL; panel vi, 50 μg/mL of blood). After 1 hour, mice were injected intradermally with PBS (site 1), 12.5 μg (site 2), and 25 μg (site 3) of anti-Ova per site. RPA was initiated by injecting Ova with 1% Evan blue intravenously through tail vein. For CD32A-Ig, 50 μg of CD32A-Ig/mL of blood was injected (panel ii). The antibody (2.4G2) treated control mice (panel iii) were injected with 25 μg/mL of blood (40 μg/mice) mAb. The PBS-injected mice served as the untreated positive control (panel i). After 3 hours the mice were killed, and the dorsal side of the skin was photographed for analysis. The figure shows 3 representative mice. (B) Quantitative analysis of RPA. The dermal lesion, shown in blue in the photographs, was quantified using ImageJ and KaleidaGraph softwares for groups with or without FcγR dimer treatment. Data are presented as the mean plus or minus the SD from 3 experiments. *P < .01, **P < .001.