Repeat administration of HPA-1a–specific antibodies provides sustained protection from HPA-1a exposure-induced FNAIT. (A) Female WT BALB/c mice from Figure 3A that had been challenged 3 weeks earlier with APLDQ platelets in the presence or absence of RLYB211 were rechallenged at day 21 with 1 × 108 APLDQ platelets with or without prior tail vein injection of additional RLYB211 or nonbinding human IgG. Blood was collected at the indicated time points, and the maternal antibodies present that were reactive against APLDQ platelets were measured by flow cytometry. Results are reported as median fluorescence intensity (MFI) (mean plus or minus SEM, n = 8-10 per group). (B-D) BALB/c female mice that had been challenged twice with APLDQ platelets in the presence or absence of RLYB211 were then bred at day 35 with APLDQ males. Approximately 21 days later, pups were born and their platelet counts determined within 48 hours of birth (mean ± SEM, n = 44-69 per group) (B). APLDQ-reactive maternal antibody levels present in the dam (mean ± SEM, n = 6-9 per group) (C) and in the pups (D) (mean ± SEM, n = 44-69 per group) were then determined by flow cytometry. Platelet counts in pups born to female mice that had been treated with either no antibody or normal human IgG served as controls. Note the dose-dependent nature of protection, beginning at ∼1 IU/mL RYLB211. Significance was determined using the Mann-Whitney U test. ∗∗P < .01; ∗∗∗P < .001; ∗∗∗∗P < .0001. nhIgG, normal human IgG; SEM, standard error of the mean.
