Figure 3
Figure 3. IL-17A enhances GVHD mortality in models using BALB/c donors. Survival by Kaplan-Meier analysis of lethally irradiated (A) B6D2F1 or (B) BALB.B mice (n = 16-20 /group) transplanted with grafts from G-CSF–mobilized B6.WT or B6.IL-17A−/− donors. G-CSF–treated TCD B6.WT grafts (n = 7 or 8) were used as non-GVHD controls. Data combined from 2 experiments for each model. Lethally irradiated (C) B6 (n = 33-35/group) or (D) DBA/2 (n = 23 or 24 /group) mice were transplanted with grafts from G-CSF–mobilized WT or IL-17A−/− BALB/c donors. G-CSF–treated TCD WT grafts (n = 12-15) were used as non-GVHD controls. **P < .001 WT vs IL-17A−/− in BALB/c → B6 model. *P < .012 WT vs IL-17A−/− in BALB/c → DBA/2 model. Data combined from 3 or 4 experiments for each model.

IL-17A enhances GVHD mortality in models using BALB/c donors. Survival by Kaplan-Meier analysis of lethally irradiated (A) B6D2F1 or (B) BALB.B mice (n = 16-20 /group) transplanted with grafts from G-CSF–mobilized B6.WT or B6.IL-17A−/− donors. G-CSF–treated TCD B6.WT grafts (n = 7 or 8) were used as non-GVHD controls. Data combined from 2 experiments for each model. Lethally irradiated (C) B6 (n = 33-35/group) or (D) DBA/2 (n = 23 or 24 /group) mice were transplanted with grafts from G-CSF–mobilized WT or IL-17A−/− BALB/c donors. G-CSF–treated TCD WT grafts (n = 12-15) were used as non-GVHD controls. **P < .001 WT vs IL-17A−/− in BALB/c → B6 model. *P < .012 WT vs IL-17A−/− in BALB/c → DBA/2 model. Data combined from 3 or 4 experiments for each model.

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