Fig. 1.
Fig. 1. Prevention of lethal acute GVHD by anti-FasL and/or anti-TNFα antibodies. Lethal acute GVHD was induced by IV injection of B6 splenocytes into CBF1 mice on days 0 and 7. Ten mice in each group received IP 2 mg anti-FasL MoAb (▴), 1 mg anti-TNFα MoAb (▵), 2 mg anti-FasL MoAb and 1 mg anti-TNFα MoAbs (•), or control IgG (○) on days 0, 4, 8, and 12. Survival (A) was monitored every day until day 56. Body weight (B) was measured at the indicated days is indicated as the mean ± standard deviation (SD) of 5 to 10 mice. In (B), the body weight of age-matched normal CBF1 (◊) is also plotted. In (A), *P < .05 and **P < .01 compared with the GVHD group. In (B), *P < .05 compared with the normal CBF1 group.

Prevention of lethal acute GVHD by anti-FasL and/or anti-TNFα antibodies. Lethal acute GVHD was induced by IV injection of B6 splenocytes into CBF1 mice on days 0 and 7. Ten mice in each group received IP 2 mg anti-FasL MoAb (▴), 1 mg anti-TNFα MoAb (▵), 2 mg anti-FasL MoAb and 1 mg anti-TNFα MoAbs (•), or control IgG (○) on days 0, 4, 8, and 12. Survival (A) was monitored every day until day 56. Body weight (B) was measured at the indicated days is indicated as the mean ± standard deviation (SD) of 5 to 10 mice. In (B), the body weight of age-matched normal CBF1 (◊) is also plotted. In (A), *P < .05 and **P < .01 compared with the GVHD group. In (B), *P < .05 compared with the normal CBF1 group.

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