(A–E) FeCl₃-induced injury of mesenteric arterioles in WT, FasR^–/–, or FasL^–/– mice (n = 5–9/group). Beginning of thrombus formation (A), time to irreversible occlusion (B), representative intravital microscopy images (C), percentage of mice with no occlusion (D) (WT vs. FasR^–/–: P = 0.0002; WT vs. FasL^–/–: P = 0.0011), and thrombus size (E) are shown. The break-off was set at 40 minutes after vessel injury when no occlusion occurred. (F–H) FeCl₃-induced injury of mesenteric arterioles in PF4-Cre⁺ FasL^fl/fl mice. PF4-Cre^– FasL^fl/fl mice served as controls. (F) Beginning of thrombus formation, (G) time to irreversible occlusion, and percentage of mice with no occlusion (H, P = 0.003) are shown (n = 8/group). (I–K) Platelet-RBC interactions after ligation of the inferior vena cava (IVC) were analyzed by intravital epifluorescence microscopy. Mice received murine platelets from C57BL/6 or FasL^–/– mice labeled with rhodamine B and murine RBCs from C57BL/6 or FasR^–/– mice labeled with DCF. (I) Number of platelet-RBC interactions per second (WT vs. FasR^–/– RBCs: P = 0.008; WT vs. FasL^–/– platelets: P = 0.072). (J) Cell interaction was quantified (90 minutes: WT vs. FasR^–/– RBCs: P = 0.003; WT vs. FasL^–/– platelets: P = 0.0163). (K) Representative images of platelet-RBC interactions in WT mice 60 minutes after IVC ligation (n = 4). Scale bar: 10 μm. (L and M) Venous thrombus formation was investigated in a flow restriction model of the IVC and thrombus weight was determined: (L) IgG vs. FasR antibody–treated mice (P = 0.2814); (M) FasL^–/– compared with WT mice (P = 0.0446). (N) Tail bleeding times were determined (n = 6/group). Data are the mean ± SEM. *P < 0.05; **P < 0.01; ***P < 0.001 by Student’s t test (F, G, and M), 1-way ANOVA with Dunnett’s multiple-comparisons test (A, B, I, J, and N), log-rank (Mantel-Cox) test (D and H), or 2-way ANOVA with Sidak’s multiple-comparisons test (E).