Interleukin-1-mediated inflammatory memory: Protective training or maladaptive tumor imprinting?

Area of Science:

• Immunology
• Hematopoiesis
• Cancer Biology

Background:

• Interleukin-1 (IL-1) is crucial for innate immunity and inflammation.
• IL-1 systemically regulates hematopoietic stem and progenitor cells (HSPCs).
• Tumors are inflammatory entities influencing hematopoiesis.

Purpose of the Study:

• To discuss IL-1 signaling in emergency myelopoiesis and inflammatory memory.
• To explore how IL-1-mediated hematopoietic reprogramming influences cancer progression.
• To highlight therapeutic strategies targeting IL-1.

Main Methods:

• Review of existing literature on IL-1 signaling in hematopoiesis and cancer.
• Analysis of IL-1's role in emergency myelopoiesis and inflammatory memory.
• Discussion of epigenetic, metabolic, and transcriptomic changes induced by IL-1.

Main Results:

• IL-1 induces durable changes in HSPCs, affecting myeloid progeny.
• IL-1 signaling contributes to an immunosuppressive phenotype in myeloid cells within tumors.
• Chronic inflammation and IL-1 signaling may promote clonal hematopoiesis and cancer susceptibility.

Conclusions:

• IL-1 signaling plays a significant role in shaping immune responses and influencing cancer progression.
• Targeting IL-1-mediated hematopoietic reprogramming offers potential therapeutic avenues.
• Understanding IL-1's systemic effects is key to managing inflammation-associated diseases and cancers.