Innate immune signaling-driven myeloid remodeling in cancer: inflammatory amplification, immune suppression, and therapeutic targeting.

Innate immune signaling is a central regulator of cancer immunity, but its effects are highly context-dependent. Acute and spatially controlled innate immune activation can promote dendritic-cell maturation, antigen presentation, and cytotoxic lymphocyte recruitment. In contrast, chronic, systemic, or therapy-induced inflammatory signaling often redirects the tumor ecosystem toward suppressive myeloid remodeling. This review discusses how innate immune pathways reshape myelopoiesis, macrophage polarization, MDSC activation, tumor-associated neutrophil recruitment, and stromal-myeloid inflammatory niches. We focus on selected signaling axes that represent distinct layers of innate inflammatory regulation, including cytokine-mediated myeloid instruction, inflammasome activation, nucleic-acid sensing, chemokine-driven recruitment, stromal transcriptional integration, and lipid-mediator signaling. These axes include IL-4/IL-4Rα, IL-1α/IL-1β, TGF-β, interferon signaling, NLRP3 inflammasome activation, STING, STAT3, IL-8/CXCR2, CCR2, and CysLTR1. These pathways can expand suppressive myeloid output from the bone marrow, reinforce tumor-associated macrophage states such as TREM2