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Viral peptide–MHC complexes are formed when short peptides derived from viral proteins are loaded onto MHC class I (primarily) or class II molecules inside infected cells and transported to the cell surface[2][6]. The primary biological function of these complexes is to present viral antigens to T cells, enabling the immune system to identify and eliminate infected cells. MHC class I–presented peptides are mostly recognized by cytotoxic T lymphocytes (CD8+), leading to targeted killing of the infected cell[4][6][2]. The diversity and specificity of these complexes arise from the polymorphism of MHC molecules and the diversity of viral peptides processed and presented[3][4]. Immune therapies increasingly leverage knowledge of peptide–MHC complexes, but challenges include immune evasion by viruses (e.g., by downregulating MHC expression) and potential triggering of autoimmunity or off-target effects in immunotherapy[6].
T cell receptor (TCR)-mediated recognition and cytotoxicity Checkpoint inhibitors enhance T cell responses to peptide–MHC Adoptive T cell therapies (TCR-T, CAR-T variants) exploit peptide–MHC recognition for specific cell killing
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