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The tumor microenvironment (TME) immune cells represent a heterogeneous collection of leukocytes that infiltrate or reside within the vicinity of a tumor, forming a dynamic ecosystem often referred to as the tumor immune microenvironment (TIME) [1.3.1, 1.3.2]. This population includes effector cells such as CD8+ cytotoxic T cells and Natural Killer (NK) cells, which are responsible for anti-tumor immunity, as well as immunosuppressive populations like regulatory T cells (Tregs), myeloid-derived suppressor cells (MDSCs), and tumor-associated macrophages (TAMs) [1.1.2, 1.4.1]. In many cancers, the TME is characterized by an immunosuppressive state where tumor cells exploit inhibitory pathways, known as checkpoints, to evade immune detection and destruction [1.1.1, 1.3.5]. Therapeutic strategies targeting these cells include immune checkpoint inhibitors (e.g., anti-PD-1/PD-L1), adoptive cell therapies like CAR-T or TIL therapy, and agents designed to deplete or reprogram suppressive myeloid cells [1.2.1, 1.3.1]. Understanding the spatial distribution, metabolic state, and functional phenotype of these immune cells is vital for predicting clinical response to immunotherapy and overcoming therapeutic resistance in solid and hematological malignancies [1.3.2, 1.4.5].
Modulation of immune checkpoints, depletion of immunosuppressive cell populations (such as TAMs and MDSCs), activation of effector T cells, and metabolic reprogramming of the microenvironment to restore anti-tumor immunity.
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