Figure 5.
Inhibition of fibrin deposition by α-FcRn antibody in a murine model of HIT. Widefield cremaster muscle arteriole laser injuries were performed in human PF4+/FcγRIIa+ mice pretreated with 200 µg per mouse of α-mouse FcRn (α-mFcRn) antibody (Ab; DVN24) or IgG2a isotype control. Three mice from each arm were studied, and each mouse had 5 to 8 injuries. Accumulations of platelets (A) and fibrin (B) in relative fluorescence units (RFUs) over time are shown. (C) Total accumulation was determined by calculating the area under the curve (AUC) for each injury. ***P < .0001 by Student t test with Welch’s correction.

Inhibition of fibrin deposition by α-FcRn antibody in a murine model of HIT. Widefield cremaster muscle arteriole laser injuries were performed in human PF4+/FcγRIIa+ mice pretreated with 200 µg per mouse of α-mouse FcRn (α-mFcRn) antibody (Ab; DVN24) or IgG2a isotype control. Three mice from each arm were studied, and each mouse had 5 to 8 injuries. Accumulations of platelets (A) and fibrin (B) in relative fluorescence units (RFUs) over time are shown. (C) Total accumulation was determined by calculating the area under the curve (AUC) for each injury. ***P < .0001 by Student t test with Welch’s correction.

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