Figure 5.
The absence of TLK2 attenuates leukemia burden and IL-1β–driven AML progression in a murine model of leukemia. (A) A schematic representation of a murine AML bone marrow transduction/transplantation model to study the effect of TLK2 deletion on leukemia progression. Lineage-depleted Tlk2+/+, Tlk2+/−, Tlk2−/− bone marrow cells were transduced with MSCV-IRES-MLL-ENL-GFP retrovirus. After 48 hours of transduction, 15 000 sorted Lin−GFP+ cells and supporting cells were injected into lethally irradiated C57BL/6 recipients. After engraftment confirmation, recipient mice were treated with 0.25 μg IL-1β or vehicle and monitored daily. (B) Kaplan-Meier survival curve of recipient mice. The log-rank test was used for statistical analysis. (C) The percentage of leukemic cells in the peripheral blood over time was measured by flow cytometry. ∗P < .05, ∗∗P < .01, and ∗∗∗∗P < .0001.

The absence of TLK2 attenuates leukemia burden and IL-1β–driven AML progression in a murine model of leukemia. (A) A schematic representation of a murine AML bone marrow transduction/transplantation model to study the effect of TLK2 deletion on leukemia progression. Lineage-depleted Tlk2+/+, Tlk2+/−, Tlk2−/− bone marrow cells were transduced with MSCV-IRES-MLL-ENL-GFP retrovirus. After 48 hours of transduction, 15 000 sorted Lin−GFP+ cells and supporting cells were injected into lethally irradiated C57BL/6 recipients. After engraftment confirmation, recipient mice were treated with 0.25 μg IL-1β or vehicle and monitored daily. (B) Kaplan-Meier survival curve of recipient mice. The log-rank test was used for statistical analysis. (C) The percentage of leukemic cells in the peripheral blood over time was measured by flow cytometry. ∗P < .05, ∗∗P < .01, and ∗∗∗∗P < .0001.

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