Myeloid cell

Myeloid cells are a broad lineage of innate immune cells, including monocytes, macrophages, dendritic cells, and granulocytes, that play a central role in tissue homeostasis and immune defense (NIH). At the cellular and tissue level, these cells are responsible for phagocytosis, antigen presentation, and the orchestration of inflammatory responses through cytokine secretion (Biocompare). In the context of the tumor microenvironment, myeloid cells often differentiate into immunosuppressive subsets, such as tumor-associated macrophages (TAMs) and myeloid-derived suppressor cells (MDSCs), which facilitate tumor progression and immune evasion (Frontiers). Therapeutic targeting of the myeloid compartment involves strategies to deplete these suppressive cells, block their recruitment via chemokine pathways, or reprogram them into pro-inflammatory phenotypes to enhance anti-tumor immunity (Springer). Drugs such as CSF1R inhibitors and CD47-SIRPα blockers are designed to modulate these cells to overcome resistance to standard immunotherapies (NIH). However, therapeutic intervention must be carefully managed to avoid systemic immunosuppression or inflammatory toxicities like cytokine release syndrome (Omnicuris).

Other names

Myeloid lineage cellMyeloid-derived cellMyeloid infiltrateMyelocyteMyeloid-derived suppressor cell (MDSC)Tumor-associated macrophage (TAM)

Therapeutic strategies targeting myeloid cells include the depletion of immunosuppressive subsets (e.g., via CSF1R inhibition), inhibition of recruitment via chemokine/receptor blockade (e.g., CCR2, CXCR2), reprogramming of cells from anti-inflammatory (M2-like) to pro-inflammatory (M1-like) phenotypes (e.g., via TLR agonists or PI3Kγ inhibition), and the blockade of myeloid-specific immune checkpoints (e.g., CD47, TREM2) to enhance phagocytosis and T-cell activation (NIH; Frontiers; Springer).