Summary: Ellegast and colleagues show that monocytic acute myeloid leukemias (AML), enriched in inflammatory and immune gene sets, exploit a transcriptional repressor—namely, IRF2BP2—to mitigate their cell-intrinsic inflammatory output and ensure their maintenance. IRF2BP2 ablation results in heightened inflammatory signals that reach a set point that triggers apoptotic AML cell death in an NF-κB–IL1β–dependent manner. The study identifies IRF2BP2 as a cell-intrinsic vulnerability with potential therapeutic significance in monocytic AML. See related article by Ellegast et al., p. 1760 (6).

中文翻译：

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走钢丝：平衡微妙的炎症反应以根除急性髓系白血病

摘要：Ellegast 及其同事表明，富含炎症和免疫基因集的单核细胞急性髓系白血病 (AML) 利用转录抑制因子（即 IRF2BP2）来减轻其细胞内在炎症输出并确保其维持。IRF2BP2 消融导致炎症信号增强，达到设定点，以 NF-κB–IL1β 依赖性方式触发凋亡性 AML 细胞死亡。该研究将 IRF2BP2 确定为一种细胞固有的脆弱性，在单核细胞 AML 中具有潜在的治疗意义。请参阅 Ellegast 等人的相关文章，第 17 页。1760（6）。