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Myeloid cells represent a diverse lineage of hematopoietic cells including monocytes, macrophages, neutrophils, and dendritic cells that originate from the bone marrow [1]. They are primary mediators of the innate immune system, functioning through phagocytosis, cytokine production, and antigen presentation to initiate adaptive immunity [2]. In the context of disease, dysregulated myeloid cells are central to chronic inflammation and the formation of the immunosuppressive tumor microenvironment, where myeloid-derived suppressor cells (MDSCs) inhibit T-cell activity [3]. Therapeutic strategies often involve targeting specific receptors on these cells, such as CD33 in acute myeloid leukemia or CSF1R to deplete tumor-associated macrophages [4]. Additionally, blockade of the CD47 'don't eat me' signal aims to enhance myeloid-mediated phagocytosis of malignant cells [5]. Because the term 'Myeloid cells' refers to an entire cell lineage rather than a single protein or receptor, it is classified as a cell population rather than a discrete molecular target [1,3]. Sources: [1] StatPearls, Hematopoiesis; [2] Janeway's Immunobiology; [3] Nature Reviews Immunology (2012, 12:253-268); [4] FDA drug labels for Gemtuzumab and Pexidartinib; [5] NEJM (2018, 379:1711-1721).
Modulation of myeloid cell activity occurs through the targeting of specific surface receptors (e.g., CD33, CSF1R, CD47) to induce antibody-dependent cellular cytotoxicity, inhibit survival signaling, or block 'don't eat me' signals to enhance phagocytosis.
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