Figure 6.
VITT Ab–induced procoagulant PLT-mediated thrombus formation can be prevented via the inhibition of SYK in PLTs. (A-B) PLTs from healthy individuals were incubated with IgG from patients with VITT in the presence of exogenous PF4 (10 μg/mL) and indicated SYK inhibitors or vehicle control (upper panel) before reconstitution into autologous PLT-depleted WB and perfusion through microfluidic channels at a venous shear rate of 250 sec–1 (10 dyne) for 25 minutes. (A) After perfusion, images were acquired at magnification ×40. Scale bar, 20 μm. (B) Violin plots showing the percentage of total (% SAC) by DiOC6, PS, fibrin(ogen), count of Hoechst-positive–labeled cells; and cumulative total % SAC of DiOC6, PS, and fibrin(ogen)-labeled thrombus captured in the microfluidic channel. Unpaired or paired t test is shown. ∗P < .05; ∗∗P < .01; ∗∗∗P < .001. N, number of patients tested; ns, nonsignificant.

VITT Ab–induced procoagulant PLT-mediated thrombus formation can be prevented via the inhibition of SYK in PLTs. (A-B) PLTs from healthy individuals were incubated with IgG from patients with VITT in the presence of exogenous PF4 (10 μg/mL) and indicated SYK inhibitors or vehicle control (upper panel) before reconstitution into autologous PLT-depleted WB and perfusion through microfluidic channels at a venous shear rate of 250 sec–1 (10 dyne) for 25 minutes. (A) After perfusion, images were acquired at magnification ×40. Scale bar, 20 μm. (B) Violin plots showing the percentage of total (% SAC) by DiOC6, PS, fibrin(ogen), count of Hoechst-positive–labeled cells; and cumulative total % SAC of DiOC6, PS, and fibrin(ogen)-labeled thrombus captured in the microfluidic channel. Unpaired or paired t test is shown. ∗P < .05; ∗∗P < .01; ∗∗∗P < .001. N, number of patients tested; ns, nonsignificant.

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