Fig. 1.
Fig. 1. Anti-CD9 antibody activates FcγRIIA tg mouse platelets in an FcγRIIA-dependent manner. / Tracings from in vitro platelet aggregometry assays are shown. Platelet aggregation is measured as light transmission over time. (A) Platelet-rich plasma (PRP) from wild-type mice treated with either anti-CD9 antibody (αCD9) at a final concentration of 40 μg/mL, in green, or treated with ADP (positive control, red) at a final concentration of 10 μmol/L shows no activation by anti-CD9. (B) PRP from FcγRIIA tg mice (F0 11) treated with 40 μg/mL αCD9, in red, or 10 μmol/L final concentration ADP (green), shows activation by anti-CD9. (C) PRP from FcγRIIA tg mice treated with 40 μg/mL antiplatelet antibody 4A5, in red, shows no activation. (D) PRP from FcγRIIA tg mice treated with 20 μg/mL αCD9 following pretreatment with 20 μg/mL IV.3, an anti-FcγRIIA antibody (green), or saline (red), shows blockade of activation by IV.3 but not saline.

Anti-CD9 antibody activates FcγRIIA tg mouse platelets in an FcγRIIA-dependent manner.

Tracings from in vitro platelet aggregometry assays are shown. Platelet aggregation is measured as light transmission over time. (A) Platelet-rich plasma (PRP) from wild-type mice treated with either anti-CD9 antibody (αCD9) at a final concentration of 40 μg/mL, in green, or treated with ADP (positive control, red) at a final concentration of 10 μmol/L shows no activation by anti-CD9. (B) PRP from FcγRIIA tg mice (F0 11) treated with 40 μg/mL αCD9, in red, or 10 μmol/L final concentration ADP (green), shows activation by anti-CD9. (C) PRP from FcγRIIA tg mice treated with 40 μg/mL antiplatelet antibody 4A5, in red, shows no activation. (D) PRP from FcγRIIA tg mice treated with 20 μg/mL αCD9 following pretreatment with 20 μg/mL IV.3, an anti-FcγRIIA antibody (green), or saline (red), shows blockade of activation by IV.3 but not saline.

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