Ameliorative effects and adverse events caused by 17C02-IgG1_OA in an antibody-mediated model of ITP. (A) FcγR-humanized mice were IV injected with 540 μM of 17C02-IgG1_OA, and body temperatures of mice were assessed for 45 minutes after treatment to investigate the inflammatory nature of the molecule (time “0” indicates before treatment). Data are presented as mean ± standard deviation (n = 6). The statistical analysis was performed by a 2-way ANOVA and Sidak multiple comparisons test (∗P < .05; ∗∗P < .01; ∗∗∗P < .001). (B) Mice were bled and platelet counts assessed 2 hours after 17C02-IgG1_OA treatment to determine the ability of the antibody itself to cause thrombocytopenia. Rabbit antiplatelet serum alone (15 μL/mouse) was used as a positive control. Data are presented as mean ± standard deviation from 3 independent experiments (n = 6). The statistical analysis was performed by a 1-way ANOVA and Tukey multiple comparisons test (∗P < .05; ∗∗∗P < .001). (C) Mice were IV injected with 15 μL of rabbit antiplatelet serum 2 hours after 17C02-IgG1_OA treatment to induce thrombocytopenia. Two hours after injection with the antiplatelet serum, mice were bled for enumeration of platelet counts to assess the ability of 17C02-IgG1_OAto ameliorate thrombocytopenia. Data are presented as mean ± standard deviation (n = 6 mice). The statistical analysis was performed by a 1-way ANOVA and Tukey multiple comparisons test (∗∗P < .01; ∗∗∗P < .001).