Myeloid cells as sources and targets of IL-1 family cytokines in cancer

Inflammation is a defining feature of the tumor microenvironment (TME) and a key driver of cancer progression. Among inflammatory mediators, the interleukin-1 (IL-1) family of cytokines serves as a central mediator linking tissue damage, metabolic stress and microbial cues to innate immune activation. Myeloid cells are major components of this network, with macrophages and neutrophils acting both as highly responsive targets of IL-1 family signaling and as important sources of IL-1 family cytokines, thereby establishing self-reinforcing inflammatory loops within tumors. Recent advances in single-cell and spatial analyses have revealed the remarkable heterogeneity of tumor-associated macrophages (TAMs) and tumor-associated neutrophils (TANs), highlighting how IL-1 family cytokines shape their recruitment, differentiation, and functional reprogramming in cancer. In turn, myeloid-derived IL-1 family cytokines contribute to inflammatory networks that influence tumor growth, immune suppression, and stromal remodeling. Here, we review the reciprocal interactions between IL-1 family cytokines/receptors and myeloid cells in cancer, focusing on how IL-1 family members instruct macrophage and neutrophil responses and how these cells shape IL-1 family-driven inflammatory circuits in the TME.