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Tumor antigen recognition is a complex immunological process rather than a single molecular target. It is the fundamental mechanism by which the adaptive immune system distinguishes malignant cells from healthy tissue, primarily mediated through the interaction between T-cell receptors (TCRs) and peptide-major histocompatibility complexes (pMHC) or through synthetic chimeric antigen receptors (CARs) binding directly to cell-surface proteins [1, 2, 4]. This process is the therapeutic basis for adoptive cell therapies (TCR-T and CAR-T), cancer vaccines, and bispecific T-cell engagers (BiTEs), which aim to redirect immune effector cells toward tumor-associated antigens (TAAs) or neoantigens [3, 4, 11]. Successful recognition triggers a cascade of signaling events leading to T-cell activation, cytokine release, and the direct lysis of tumor cells via perforins and granzymes [5, 7]. Pharmaceutical intervention in this area focuses on enhancing the affinity and specificity of this recognition to maximize anti-tumor efficacy while minimizing off-target effects [3, 9, 11].
Facilitation or engineering of high-affinity binding between immune effector cells and tumor-specific or tumor-associated antigens to induce cytotoxic cell death.
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