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Immunosuppressive cells in the tumor microenvironment (TME) represent a heterogeneous collection of immune and non-immune cells that collectively inhibit the host's anti-tumor immune response [1]. This population primarily includes regulatory T cells (Tregs), myeloid-derived suppressor cells (MDSCs), and M2-polarized tumor-associated macrophages (TAMs), which utilize various mechanisms such as the secretion of inhibitory cytokines (e.g., TGF-beta, IL-10) and the expression of immune checkpoints to create a permissive environment for tumor growth and metastasis [1, 2]. In the context of oncology, these cells are not a single molecular target but rather a therapeutic compartment; drugs are designed to either deplete these populations, block their recruitment, or reprogram them from pro-tumor to anti-tumor phenotypes [3, 4]. For example, CSF1R inhibitors target TAMs, while CTLA-4 antagonists can deplete intratumoral Tregs [3, 4]. Understanding the composition and function of these cells is critical for overcoming resistance to immunotherapy and improving patient outcomes in various malignancies [1].
Depletion of suppressive cell populations, inhibition of suppressive cytokines, blockade of recruitment to the tumor site, and phenotypic reprogramming from immunosuppressive to immunostimulatory states.
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