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The term antitumor immune response refers broadly to the collective actions by which components of the host's innate and adaptive immunity recognize and eliminate cancerous cells. This process involves multiple cell types—most notably cytotoxic T lymphocytes, natural killer cells, dendritic cells—and is shaped by interactions within the tumor microenvironment. The effectiveness of this natural defense can be undermined by various mechanisms employed by tumors such as downregulation of antigen presentation machinery, secretion of immunosuppressive factors, recruitment of regulatory T cells or myeloid-derived suppressors, and establishment of an immunosuppressive stroma. While not itself a druggable molecular entity like a receptor or enzyme, understanding and manipulating elements that govern the antitumor immune response forms the basis for modern cancer immunotherapies—including checkpoint blockade agents—which aim to restore or amplify these endogenous defenses against malignancy.
For drugs that enhance the antitumor immune response: Blockade of inhibitory pathways on T cells (e.g., PD-1/PD-L1, CTLA4 inhibitors); Activation of effector lymphocytes against tumor cells; Enhancement of antigen presentation and co-stimulation in the tumor microenvironment
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