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<p>Acute myeloid leukemia (AML) is a heterogenous disease characterized by the accumulation of immature myeloid blasts with distinct genetic mutations in the bone marrow and peripheral blood. AML co-evolve with other components of specialized bone marrow niches within a microenvironment enriched in cytokines and inflammatory cells; among these, interleukin-1 (IL-1) may act as a tumor driver. This review examines two complementary aspects of AML biology in relation to IL-1. First, we describe the functional activity of IL-1 and the signaling pathways triggered by the IL-1 receptor in malignant cells, along with preclinical and clinical studies targeting this pathway in AML. Second, we discuss the mechanisms regulating the release of mature IL-1β through the activation of different inflammasomes. Inflammasomes, particularly NLRP3, are emerging as key contributors to AML pathophysiology. Beyond IL-1 release, NLRP3 may interface with cellular stress responses and pyroptosis, thereby influencing both AML cells and their microenvironment through multiple mechanisms. Inflammasome signaling may act as a driver of therapy resistance while also representing a promising therapeutic target.</p>

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IL-1 signaling and inflammasomes in acute myeloid leukemia: mechanisms and therapeutic opportunities

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月19日

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  • Alessandra Mortellaro,
  • Sara Mastaglio,
  • Marta Muzio

摘要

Acute myeloid leukemia (AML) is a heterogenous disease characterized by the accumulation of immature myeloid blasts with distinct genetic mutations in the bone marrow and peripheral blood. AML co-evolve with other components of specialized bone marrow niches within a microenvironment enriched in cytokines and inflammatory cells; among these, interleukin-1 (IL-1) may act as a tumor driver. This review examines two complementary aspects of AML biology in relation to IL-1. First, we describe the functional activity of IL-1 and the signaling pathways triggered by the IL-1 receptor in malignant cells, along with preclinical and clinical studies targeting this pathway in AML. Second, we discuss the mechanisms regulating the release of mature IL-1β through the activation of different inflammasomes. Inflammasomes, particularly NLRP3, are emerging as key contributors to AML pathophysiology. Beyond IL-1 release, NLRP3 may interface with cellular stress responses and pyroptosis, thereby influencing both AML cells and their microenvironment through multiple mechanisms. Inflammasome signaling may act as a driver of therapy resistance while also representing a promising therapeutic target.