Immunologic depletion of NK cells establishes NK cell–independent mechanism coupling both TF and prothrombin to metastatic success. (A) Comparative analysis of residual [¹²⁵I] -radiolabeled TF^WT cells present in the lungs of cohorts of fibrinogen deficient (Fib⁻) and control (Fib⁺) mice pretreated with either an anti-NK Ig (antiasialo GM₁) known to deplete NK cells (n = 11 for each genotype) or nonimmune IgG (n = 12 for each genotype) harvested 24 hours after intravenous injection of 1 × 10⁵ tumor cells. Note that immunologic depletion of NK cells, like genetic depletion of NK cells, eliminates fibrin(ogen) as a determinant of the early survival of TF^WT cells. (B) Quantitative analysis of residual [¹²⁵I] -radiolabeled TF^WT cells (n = 5-6 for each group) in the lungs of Gαq⁺ and Gαq⁻ mice. Note that platelet function, like fibrinogen, ceases to be a determinant of the early survival of TF^WT cells in mice immunologically depleted of NK cells. (C) Comparative analysis of residual [¹²⁵I] -radiolabeled TF^WT (black bars) or TF^O cells (white bars) cells (n = 6-7 for each group) in the lungs 24 hours after injection of 10⁵ tumor cells. Note that tumor cell-associated TF remains a significant determinant of early tumor cell survival even in mice immunologically depleted of NK cells. (D) Quantitative analysis of residual [¹²⁵I] -radiolabeled TF^WT cells (n = 6-7 for each group) in the lungs of fII^Low and control mice. Note that circulating prothrombin levels, like tumor cell TF expression, remain a significant determinant of early tumor cell survival even after the immunologic depletion of NK cells. All P values were generated with the Mann Whitney U test. The error bars represent SEM.