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Immunosuppressive myeloid cells in the tumor microenvironment comprise a heterogeneous mix of immature and differentiated myeloid cells, such as myeloid-derived suppressor cells (MDSCs), tumor-associated macrophages (TAMs), neutrophils, and dendritic cells. These cell populations are recruited and reprogrammed by tumor and stromal factors to inhibit host anti-tumor immunity, promote tumor angiogenesis, and facilitate metastatic spread. Modulating these cells—either by depleting them, blocking their immunosuppressive effects, or altering their differentiation pathways—is an emerging therapeutic strategy in cancer. Targeting specific molecules or pathways in these cells (e.g., immune checkpoints, chemokine receptors) can potentially enhance anti-tumor immunity, but is complicated by cell heterogeneity, compensatory mechanisms, and risk of systemic immune-related side effects
Inhibition of immunosuppressive signaling (e.g., checkpoint blockade restores immune function) Depletion or reprogramming of myeloid cells Modulation of cytokine signaling
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