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The interface between the **T cell receptor (TCR)** on T lymphocytes and the **peptide–major histocompatibility complex (pMHC)** complex presented on dendritic cells is the fundamental recognition event that initiates adaptive cellular immunity[1][3][4][5][7]. The TCR scans and binds peptide antigens nestled within the MHC groove; these peptides may be derived from pathogens, tumors, or self-proteins. Dendritic cells, as professional antigen-presenting cells, display peptide fragments in the context of MHC class I or II molecules depending on the antigen source and processing pathway. The engagement of the TCR with its cognate pMHC ligand triggers intracellular signaling cascades, activating T cells and directing the nature and magnitude of the immune response. Defects or dysregulation at this interface underlie numerous pathological conditions, including autoimmune diseases, cancers, and immunodeficiencies. This interaction is a central target for immunotherapies and vaccines, leveraging cellular immunity for disease control and eradication[1][3][5][7].
Induction or inhibition of TCR–pMHC interaction to activate or dampen T cell responses Modulation of antigen presentation (MHC loading, stabilization, or alteration) Blocking or mimicking pMHC engagement to influence TCR signaling Genetic modification to re-target T cells (TCR gene transfer therapies)
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