Figure 6.
Figure 6. Absence of IAPs in host target tissues plays an important role in aggravating GVHD. To make BM chimeras, B6-WT, B6-cIAP1−/−, and B6-XIAP−/− animals were lethally irradiated with 10 Gy and infused with 5 × 106 BM cells and 5 × 106 splenocytes from syngeneic B6Ly5.2 donors. Three to 4 months later, B6 Ly5.2→B6, B6Ly5.2→cIAP1−/−, and B6Ly5.2→XIAP−/− animals were irradiated with 9 Gy and received 3 × 106 CD90+ T cells along with 5 × 106 TCD-BM cells from either syngeneic B6 or allogeneic MHC-mismatched BALB/c donors. (A-B) Survival. ***P < .001 or **P < .01, when allogeneic B6Ly5.2→B6 vs B6Ly5.2→XIAP−/− animals or allogeneic B6Ly5.2→B6 vs B6Ly5.2→cIAP−/− animals were compared (n = 9-27 per group, pooled from 3 to 4 independent experiments). The bar shows the mean ± SEM.

Absence of IAPs in host target tissues plays an important role in aggravating GVHD. To make BM chimeras, B6-WT, B6-cIAP1−/−, and B6-XIAP−/− animals were lethally irradiated with 10 Gy and infused with 5 × 106 BM cells and 5 × 106 splenocytes from syngeneic B6Ly5.2 donors. Three to 4 months later, B6 Ly5.2→B6, B6Ly5.2→cIAP1−/−, and B6Ly5.2→XIAP−/− animals were irradiated with 9 Gy and received 3 × 106 CD90+ T cells along with 5 × 106 TCD-BM cells from either syngeneic B6 or allogeneic MHC-mismatched BALB/c donors. (A-B) Survival. ***P < .001 or **P < .01, when allogeneic B6Ly5.2→B6 vs B6Ly5.2→XIAP−/− animals or allogeneic B6Ly5.2→B6 vs B6Ly5.2→cIAP−/− animals were compared (n = 9-27 per group, pooled from 3 to 4 independent experiments). The bar shows the mean ± SEM.

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