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Tumor cells and antigen-presenting cells (APCs) represent a complex cellular interface rather than a single molecular therapeutic target. APCs, such as dendritic cells and macrophages, are responsible for capturing tumor-associated antigens and presenting them via Major Histocompatibility Complex (MHC) molecules to T cells to initiate an adaptive immune response (Janeway's Immunobiology). However, tumor cells frequently develop mechanisms to evade this immune detection, such as the upregulation of inhibitory ligands like PD-L1 or the active suppression of MHC expression (Hanahan and Weinberg, Cell 2011). Many modern immunotherapies, including checkpoint inhibitors like pembrolizumab and nivolumab, function by blocking the inhibitory signals exchanged between these two cell populations to enhance the body's ability to recognize and destroy malignant tissue (Pardoll, Nat Rev Cancer 2012). Because this entry describes a broad cellular environment involving multiple distinct proteins and pathways, it is classified as a cellular population rather than a specific molecular target. Understanding the spatial and functional relationship between these cells is vital for the development of cancer vaccines and adoptive cell therapies.
Modulation of immune checkpoint signaling (e.g., PD-1/PD-L1 and CTLA-4 pathways) and antigen presentation mechanisms at the cellular interface to restore anti-tumor T-cell activity.
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