Tumor-associated macrophages (TAMs)

Chronic inflammation initially drives the polarization of macrophages towards the M1 phenotype, which are pro-inflammatory and typically work to destroy pathogens and damaged cells. However, when inflammation becomes prolonged, these M1 macrophages can shift to an M2 phenotype, which is more anti-inflammatory and immunosuppressive. This shift marks a critical turning point, as the M2 macrophages begin to support tissue repair and promote an environment conducive to tumor formation. In chronic inflammation, the combination of various growth factors and cytokines, such as IL-10 and TGF-β, creates conditions that not only enable tumor cells to emerge but also allow the M2 macrophages to facilitate tumor expansion and maintain tumor homeostasis. Each stage of this transition—from M1 to M2 polarization and the subsequent support of tumor growth—is driven by distinct molecular signals and factors, contributing to a tumor microenvironment that thrives on inflammation and immune evasion.