Exogenous IFN-γ failure to rescue T-bet^−/− LN-cell functional deficiency. In 2 experiments, we attempted to use exogenous IFN-γ to restore the ability for T-bet^−/− LN cells to induce BM failure through intravenous and intraperitoneal injection. Injection of IFN-γ intraperitoneally once per day at 0.2 μg/mouse (6666 pg/g of body weight) from day 1 to day 11 to TBI-treated F1 recipients, with or without the infusion of 5 × 10⁶ T-bet^−/− LN cells, reduced recipient neutrophils without showing any effect on red blood cells, platelets, or total BM cells (A). In 2 separate experiments, we infused T-bet^−/− LN cells into sublethally irradiated CByB6F1 mice that were each installed with an osmotic pump to provide continuous infusion of IFN-γ as detailed in “Induction of BM failure.” After 12 days, plasma IFN-γ concentrations were drastically greater in mice that received IFN-γ infusion (B). Mice that received T-bet^−/− LN cells and continuous IFN-γ infusion had lower levels of WBCs, neutrophils, red blood cells, and BM cells than did mice that had received T-bet^−/− LN cells without IFN-γ (C). Data shown are means with SEs for each group: B6 LN (n = 7), T-bet^−/− LN (n = 9), T-bet^−/− LN IFN-γ (n = 9), TBI-IFN-γ (n = 4), and TBI only (n = 4).