Figure 1.
Figure 1. miR-17-92 expressed on donor T and B cells contributes to the pathogenesis of cGVHD. BALB/c (H2Kb+) mice were lethally irradiated and transferred with 0.5 × 106 splenocytes plus 2.5 × 106 TCD-BM from Cre−, CD4Cre+, CD19Cre+, and CD4 Cre+CD19Cre+ miR-17-92flox/flox mice on a C57BL/6 background. Survival (A) and clinical scores of cGVHD manifestations (B) were monitored weekly. Representative flow figures (C) and percentage (D) of CD4+CD8+ cells in recipient thymus are shown on gated donor cells 60 days post-BMT (N = 15-20 mice per group). (E) Pathology scores in recipient skin are shown 60 days post-BMT (N = 4-5 mice per group). *P < .05; **P < .01; ***P < .001.

miR-17-92 expressed on donor T and B cells contributes to the pathogenesis of cGVHD. BALB/c (H2Kb+) mice were lethally irradiated and transferred with 0.5 × 106 splenocytes plus 2.5 × 106 TCD-BM from Cre, CD4Cre+, CD19Cre+, and CD4 Cre+CD19Cre+ miR-17-92flox/flox mice on a C57BL/6 background. Survival (A) and clinical scores of cGVHD manifestations (B) were monitored weekly. Representative flow figures (C) and percentage (D) of CD4+CD8+ cells in recipient thymus are shown on gated donor cells 60 days post-BMT (N = 15-20 mice per group). (E) Pathology scores in recipient skin are shown 60 days post-BMT (N = 4-5 mice per group). *P < .05; **P < .01; ***P < .001.

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