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The **major histocompatibility complex (MHC)–antigen complex: T-cell receptor (TCR)** refers to the critical molecular interaction at the heart of adaptive immunity. An antigen-presenting cell displays a peptide antigen bound to an MHC class I or II protein on its surface. T cells recognize these peptide–MHC (pMHC) complexes via their highly diverse clonotypic TCRs. This binding triggers intracellular signaling in T cells, leading to immune activation or tolerance depending on additional contextual cues. The specificity of immune responses, self–nonself discrimination, and most forms of T cell–mediated immunity depend on this interaction. Aberrations in the process are implicated in autoimmunity, infection, cancer, and transplant rejection. Therapies targeting this axis include checkpoint inhibitors, TCR-engineered cell therapies, and vaccines[4][1][3][6][2]. **Note:** For structured databases, it is strongly recommended to separately list "T-cell receptor (TCR)" and "Major histocompatibility complex (MHC)" as drug targets, not as a combined entry, unless specific to biophysical studies or cellular immunology assays.
Blockade of immune checkpoint molecules to restore TCR signaling Antigen modulation to promote or prevent TCR:MHC interaction (e.g., cancer vaccines) Engineered TCRs to enhance recognition of tumor-specific or viral peptides TCR-mimic antibodies: bind peptide–MHC complexes and activate immune responses Peptide antagonists can block TCR engagement
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