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Immunosuppressive myeloid cells, primarily comprising myeloid-derived suppressor cells (MDSCs) and tumor-associated macrophages (TAMs), are a heterogeneous population of cells that accumulate in the tumor microenvironment (TME) to promote cancer progression (Gabrilovich, 2017). These cells exert potent inhibitory effects on anti-tumor immunity by suppressing T-cell and natural killer (NK) cell activity through the production of reactive oxygen species (ROS), arginase-1, and immunosuppressive cytokines like IL-10 and TGF-beta (Hegde et al., 2021). Beyond immune evasion, they contribute to tumor growth by stimulating angiogenesis, facilitating epithelial-mesenchymal transition (EMT), and promoting metastatic spread (Cassetta & Pollard, 2018). In clinical oncology, these cells are significant drivers of resistance to conventional therapies and modern immune checkpoint inhibitors. Therapeutic targeting of these cells involves strategies to deplete their numbers, block their recruitment via chemokine signaling (e.g., CCR2/CCL2 or CXCR2/CXCL8 axes), or pharmacologically re-educate them toward a pro-inflammatory, anti-tumor phenotype (Hegde et al., 2021). Monitoring these populations via surface markers like CD11b and CD33 is increasingly used to assess the immune landscape of tumors and predict patient response to immunotherapy.
Therapeutic strategies include the depletion of these cell populations, inhibition of their recruitment from the bone marrow to the tumor site, and functional reprogramming from a pro-tumorigenic (M2-like) to an anti-tumorigenic (M1-like) phenotype (Hegde et al., 2021).
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