Figure 3.
Administration of HPA-1a–specific antibodies prevents HPA-1a exposure-induced alloimmunization. (A-B) Female WT BALB/c mice either received 2 mg of normal human IgG, 0.25, 1.0, 4 IU/mL of RLYB211 (A) or 1.34 μg ZB007 (normal human IgG), or 1.2, 4.0, 12.0, 40.0 IU/mL of RLYB212 (B) 1 hour before transfusion of 1 × 108 APLDQ murine platelets. Blood was collected at the indicated time points, and the antibodies present that were reactive against APLDQ platelets were measured by flow cytometry. Results are reported as median fluorescence intensity (MFI) (mean ± standard error of the mean, n = 7-12 per group). Note the dose-dependent prevention of HPA-1a–induced alloimmunization, with nearly complete protection beginning at 1 IU/mL of polyclonal RLYB211 and at 4 IU/mL of monoclonal RLYB212. ∗P < .05; ∗∗P < .01; ∗∗∗P < .001 vs normal human IgG as analyzed by the Mann-Whitney U test. nhIgG, normal human IgG; ns, not significant.

Administration of HPA-1a–specific antibodies prevents HPA-1a exposure-induced alloimmunization. (A-B) Female WT BALB/c mice either received 2 mg of normal human IgG, 0.25, 1.0, 4 IU/mL of RLYB211 (A) or 1.34 μg ZB007 (normal human IgG), or 1.2, 4.0, 12.0, 40.0 IU/mL of RLYB212 (B) 1 hour before transfusion of 1 × 108 APLDQ murine platelets. Blood was collected at the indicated time points, and the antibodies present that were reactive against APLDQ platelets were measured by flow cytometry. Results are reported as median fluorescence intensity (MFI) (mean ± standard error of the mean, n = 7-12 per group). Note the dose-dependent prevention of HPA-1a–induced alloimmunization, with nearly complete protection beginning at 1 IU/mL of polyclonal RLYB211 and at 4 IU/mL of monoclonal RLYB212. ∗P < .05; ∗∗P < .01; ∗∗∗P < .001 vs normal human IgG as analyzed by the Mann-Whitney U test. nhIgG, normal human IgG; ns, not significant.

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