Extended Data Fig. 7: GPIIb/IIIa-bockade does not prevent INU1-IgG induced platelet consumption. | Nature Cardiovascular Research

Extended Data Fig. 7: GPIIb/IIIa-bockade does not prevent INU1-IgG induced platelet consumption.

From: Foudroyant cerebral venous (sinus) thrombosis triggered through CLEC-2 and GPIIb/IIIa dependent platelet activation

Extended Data Fig. 7

a. GPIIb/IIIa-blockade by JON/A-F(ab)2 treatment (2.0 µg/g i.v.) was confirmed by the absence of JON/AFITC binding using flow cytometry 20 min after JON/A-F(ab)2-treatment (n = 8 mice per group). b. Flow cytometric analysis of platelets isolated from untreated WT mice (control, n = 8) and mice pre-treated with JON/A-F(ab)2 (2.0 µg/g; 10 min before INU1-fab challenge, n = 7) 20 min after INU1-fab treatment (0.5 µg/g, i.v.). Absence of INU1FITC binding confirms the presence of INU1-fab on the circulating platelets despite unaltered platelet counts in these animals (see Fig. 3a). c. In contrast to INU1-fab induced platelet consumption, GPIIb/IIIa-blockade (2.0 µg/g JON/A-F(ab)2 i.v.) does not prevent INU1-IgG induced platelet consumption, as demonstrated by the markedly reduced platelet counts of vehicle or JON/A-F(ab)2-pretreated animals 20 min after INU1-IgG (0.75 µg/g i.v.; n = 4 mice per group). Each symbol represents one individual, the box plots depict median and minimum to maximum.

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