Figure 3.
scIV.3-IdeS inhibits IgG-mediated platelet aggregation more potently than scIV.3 alone. (A) PRP was incubated with scIV.3 (20 nM), scIV.3-IdeS (20 nM), or control and then stimulated with a mouse (Ms) anti-human CD9 antibody (Ms anti-hCD9; 1 μg/mL), ADP (20 μM), or collagen (1 μg/mL). Representative tracings for Ms anti-hCD9– and collagen-stimulated platelets were included, and maximum aggregation for 3 to 4 independent experiments was reported. (B) Washed platelets treated with 1, 2.5, or 20 nM of scIV.3 or scIV.3-IdeS were stimulated with Ms anti-hCD9 (1 μg/mL), and maximum aggregation was reported. (C) Platelets treated with predetermined concentrations of scIV.3 or scIV.3-IdeS were stimulated with rabbit (rb) anti-hCD9 (1 μg/mL), and maximum aggregation was reported (data shown as mean ± SD; 1-way analysis of variance; n = 3-4). #P < .05 (statistical difference between treated and control [0 nm]), ****P < .0001.

scIV.3-IdeS inhibits IgG-mediated platelet aggregation more potently than scIV.3 alone. (A) PRP was incubated with scIV.3 (20 nM), scIV.3-IdeS (20 nM), or control and then stimulated with a mouse (Ms) anti-human CD9 antibody (Ms anti-hCD9; 1 μg/mL), ADP (20 μM), or collagen (1 μg/mL). Representative tracings for Ms anti-hCD9– and collagen-stimulated platelets were included, and maximum aggregation for 3 to 4 independent experiments was reported. (B) Washed platelets treated with 1, 2.5, or 20 nM of scIV.3 or scIV.3-IdeS were stimulated with Ms anti-hCD9 (1 μg/mL), and maximum aggregation was reported. (C) Platelets treated with predetermined concentrations of scIV.3 or scIV.3-IdeS were stimulated with rabbit (rb) anti-hCD9 (1 μg/mL), and maximum aggregation was reported (data shown as mean ± SD; 1-way analysis of variance; n = 3-4). #P < .05 (statistical difference between treated and control [0 nm]), ****P < .0001.

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