Figure 2.
Figure 2. Acute MCMV infection induces type 1 IFN that impairs tolerance induction by donor ECDI-SPs. (A) Kinetics of serum IFN-α level post–MCMV infection (N = 4-6, compiled from 4 independent experiments). (B) Schematic treatment plan and percent graft survival with anti-IFNAR1-Ab blockade. Two cohorts of ECDI-SP–treated transplant recipients were infected with Δm157 on the day of transplantation. The first cohort additionally received anti-IFNAR1 blocking antibody (IP injection; 250 µg/mouse per day) on the indicated days, while the other cohort additionally received isotype antibody on the same indicated days (N = 5-7, compiled from 3 independent experiments). (C) Schematic treatment plan and percent graft survival with recombinant IFN-α treatment. Two cohorts of ECDI-SP–treated transplant recipients were additionally treated with vehicle (PBS) or mouse recombinant IFN-α (400 U/g per day) on the indicated days (N = 6, compiled from 2 independent experiments). *P < .05 (log-rank test).

Acute MCMV infection induces type 1 IFN that impairs tolerance induction by donor ECDI-SPs. (A) Kinetics of serum IFN-α level post–MCMV infection (N = 4-6, compiled from 4 independent experiments). (B) Schematic treatment plan and percent graft survival with anti-IFNAR1-Ab blockade. Two cohorts of ECDI-SP–treated transplant recipients were infected with Δm157 on the day of transplantation. The first cohort additionally received anti-IFNAR1 blocking antibody (IP injection; 250 µg/mouse per day) on the indicated days, while the other cohort additionally received isotype antibody on the same indicated days (N = 5-7, compiled from 3 independent experiments). (C) Schematic treatment plan and percent graft survival with recombinant IFN-α treatment. Two cohorts of ECDI-SP–treated transplant recipients were additionally treated with vehicle (PBS) or mouse recombinant IFN-α (400 U/g per day) on the indicated days (N = 6, compiled from 2 independent experiments). *P < .05 (log-rank test).

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