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Immune escape mechanisms of tumor cells encompass a variety of molecular and cellular strategies by which malignant cells evade immune detection and elimination. These include downregulation or complete loss of major histocompatibility complex (MHC) class I molecules, decreased tumor-associated antigen expression, secretion of immunosuppressive cytokines, recruitment and activation of immunosuppressive immune cell populations (such as regulatory T cells, myeloid-derived suppressor cells, and M2 macrophages), and expression of immune checkpoint ligands like PD-L1. Important molecular interactions include those between CD24 on tumor cells and Siglec-10 on immune cells, which can inhibit immune cell activation. These escape processes are major contributors to tumor progression, metastatic spread, and resistance to immunotherapies, making them a central focus for drug development aimed at modulating or reactivating anti-tumor immune responses. However, as these mechanisms represent a collection of pathways rather than a single target, the term is not appropriate for structured database entries of molecular therapeutic targets.
Blocking immune checkpoints (PD-1/PD-L1, CTLA-4) to restore anti-tumor immunity Interfering with suppressive signaling (e.g., blocking CD24–Siglec-10 interaction) Reprogramming the tumor microenvironment
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