Figure 2.
Neuraminidase treatment enhanced HPA-9b alloantibody binding. (A) Schematic of HPA-9 alloantigen and nearby O-glycans. (B) Reactions of anti-HPA-9b patient sera with HPA-9 allele-specific iPSC-derived MKs in the presence or absence of neuraminidase treatment in flow cytometry analysis. Color-coded numbers indicate median fluorescence intensity of corresponding peaks. Binding to HPA-9a cells serves as background binding for individual patient sample. Only P1 serum shows increased background binding to HPA-9a cells after neuraminidase treatment, which may be caused by the presence of unknown anti-carbohydrate antibody against certain desialylated glycan in this case. NeuAc, N-acetylneuraminic acid; Gal, galactose; GalNAc, N-acetyl-D-galactosamine; IgG, immunoglobulin G; Neu, neuraminidase; PE, phycoerythrin.

Neuraminidase treatment enhanced HPA-9b alloantibody binding. (A) Schematic of HPA-9 alloantigen and nearby O-glycans. (B) Reactions of anti-HPA-9b patient sera with HPA-9 allele-specific iPSC-derived MKs in the presence or absence of neuraminidase treatment in flow cytometry analysis. Color-coded numbers indicate median fluorescence intensity of corresponding peaks. Binding to HPA-9a cells serves as background binding for individual patient sample. Only P1 serum shows increased background binding to HPA-9a cells after neuraminidase treatment, which may be caused by the presence of unknown anti-carbohydrate antibody against certain desialylated glycan in this case. NeuAc, N-acetylneuraminic acid; Gal, galactose; GalNAc, N-acetyl-D-galactosamine; IgG, immunoglobulin G; Neu, neuraminidase; PE, phycoerythrin.

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