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Tumor-associated antigens presented by major histocompatibility complex (MHC) molecules on cancer cells comprise a heterogeneous group of peptides derived from mutated proteins (neoantigens), aberrantly expressed proteins, viral antigens, or tissue differentiation antigens produced by cancer cells[2][3][4]. These antigens are processed intracellularly and loaded onto **MHC class I** (and, less frequently, **MHC class II**) molecules, then displayed on the cell surface, where they can be recognized by T cells—especially cytotoxic CD8+ T cells for MHC I and CD4+ T cells for MHC II[1][4][5]. Recognition of these peptide–MHC complexes by T cell receptors (TCRs) is the principal initiating event for cancer cell immune elimination. Loss or alteration of **MHC-mediated antigen presentation** is a central mechanism of immune evasion in many tumors and is associated with resistance to immunotherapies such as checkpoint inhibitors[1]. Tumor antigens are the molecular foundation for a wide range of cancer immunotherapies, including TCR-engineered T cells, vaccines targeting neoantigens, and antibodies against tumor-specific antigens. Clinical translation remains challenging due to antigen heterogeneity, risk of autoimmune effects, and tumor immune escape, necessitating ongoing research for optimal antigen selection and delivery[1][2][3][4].
Immune checkpoint inhibition (restores T cell activity against antigen-presenting tumor cells)[1]; T cell activation via recognition of antigen–MHC complex; Direct cytotoxicity by TCR- or antibody-based recognition of tumor-associated peptides; Vaccine-induced expansion of antigen-specific T cells
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