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Myeloid-derived suppressor cell (MDSC) markers are a set of phenotypic indicators used to identify a heterogeneous population of immature myeloid cells that possess strong immunosuppressive capabilities. In humans, these cells are typically characterized by the expression of the myeloid markers CD11b and CD33, while lacking the expression of the MHC class II molecule HLA-DR and other lineage-specific markers (CD3, CD19, CD56) [1, 2]. MDSCs are further classified into monocytic (M-MDSC, CD14+) and polymorphonuclear (PMN-MDSC, CD15+ or CD66b+) subsets, with Lectin-type oxidized LDL receptor 1 (LOX-1) serving as a specific marker for human PMN-MDSCs [2]. These cells accumulate in the blood and tumor tissues of cancer patients, where they suppress T-cell activation and proliferation through the production of arginase-1 (ARG1), inducible nitric oxide synthase (iNOS), and reactive oxygen species (ROS) [1, 3]. Therapeutic interventions targeting MDSCs aim to deplete these cells (e.g., using gemcitabine), inhibit their recruitment to the tumor site, or induce their differentiation into mature, non-suppressive myeloid cells using agents like all-trans retinoic acid (ATRA) [3, 4]. Additionally, specific markers such as CD38 are being explored as direct therapeutic targets to deplete MDSCs and restore anti-tumor immunity [5]. Consequently, MDSC markers serve as vital tools for both the characterization of the immune landscape in cancer patients and the development of targeted therapies to overcome immune resistance [1, 3].
Therapeutic strategies involve the depletion of MDSC populations via cytotoxicity, induction of myeloid differentiation into non-suppressive mature cells, and inhibition of immunosuppressive enzymatic activities such as arginase-1 and iNOS [3, 4].
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