Figure 5
Figure 5. mAb pairs produce different patterns of inhibition when tested for their ability to block binding of patient Abs. Platelets pretreated with eptifibatide or tirofiban were incubated with saturating quantities of one of 10 “blocking” mAbs. The signal (median fluorescence intensity) obtained with a patient Ab was then determined by flow cytometry, and was expressed as a percentage of the signal obtained in the absence of a blocking mAb (percentage of relative binding). (Top panel) The eptifibatide-dependent Ab E2 was blocked almost completely by mAb pairs 10E5/290.5 and 312.2/312.8 specific for the αIIb β propeller and by 7E3, but was relatively unaffected by the other 5 mAbs. (Bottom panel) In contrast, the tirofiban-dependent Ab T2 was completely blocked by 7E3/AP2 but not by the other 4 pairs of monoclonals. Values shown are the average of triplicate measurements. Brackets indicate ± 1.0 SD.

mAb pairs produce different patterns of inhibition when tested for their ability to block binding of patient Abs. Platelets pretreated with eptifibatide or tirofiban were incubated with saturating quantities of one of 10 “blocking” mAbs. The signal (median fluorescence intensity) obtained with a patient Ab was then determined by flow cytometry, and was expressed as a percentage of the signal obtained in the absence of a blocking mAb (percentage of relative binding). (Top panel) The eptifibatide-dependent Ab E2 was blocked almost completely by mAb pairs 10E5/290.5 and 312.2/312.8 specific for the αIIb β propeller and by 7E3, but was relatively unaffected by the other 5 mAbs. (Bottom panel) In contrast, the tirofiban-dependent Ab T2 was completely blocked by 7E3/AP2 but not by the other 4 pairs of monoclonals. Values shown are the average of triplicate measurements. Brackets indicate ± 1.0 SD.

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