Fig. 5.
Fig. 5. Effects of GPIIb-IIIa antagonists and nonlabeled OP-G2 on the binding of mAbs and PA autoantibodies against GPIIb-IIIa. / (A) Effects on the binding of biotinylated mAbs AP3 and OP-G2. (B) Effects on the binding of PA autoantibodies from 6 patients with ITP. PA autoantibodies from patients 1, 3, and 8 showed the impaired binding to KO variant GPIIb-IIIa, whereas those from patients 2, 7, and 12 equally reacted with KO variant and WT GPIIb-IIIa. The binding of mAbs or PA autoantibodies in the presence of 1 mM RGDW (sparsely dotted columns), 10 μM FK506 (densely dotted columns), 10 μM Ro44-5883 (checkered columns), or 10 μg/mL nonlabeled OPG2 (solid columns) were examined in antigen-capture ELISA. Open columns represent ΔOD values in the absence of the inhibitors. ΔOD is [OD value obtained from a test sample − (mean + 3 SD) OD value obtained from 5 control samples].

Effects of GPIIb-IIIa antagonists and nonlabeled OP-G2 on the binding of mAbs and PA autoantibodies against GPIIb-IIIa.

(A) Effects on the binding of biotinylated mAbs AP3 and OP-G2. (B) Effects on the binding of PA autoantibodies from 6 patients with ITP. PA autoantibodies from patients 1, 3, and 8 showed the impaired binding to KO variant GPIIb-IIIa, whereas those from patients 2, 7, and 12 equally reacted with KO variant and WT GPIIb-IIIa. The binding of mAbs or PA autoantibodies in the presence of 1 mM RGDW (sparsely dotted columns), 10 μM FK506 (densely dotted columns), 10 μM Ro44-5883 (checkered columns), or 10 μg/mL nonlabeled OPG2 (solid columns) were examined in antigen-capture ELISA. Open columns represent ΔOD values in the absence of the inhibitors. ΔOD is [OD value obtained from a test sample − (mean + 3 SD) OD value obtained from 5 control samples].

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