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Peptide-Major Histocompatibility Complex (pMHC) complexes presenting Cytomegalovirus (CMV) antigens are essential targets for the cellular immune response against CMV infection (PubMed: 15596815). These complexes are formed when viral proteins, such as the tegument protein pp65 or the immediate-early protein IE1, are processed into short peptides and loaded onto MHC Class I molecules within the host cell (PubMed: 11748273). Once displayed on the surface of CMV-infected cells, these pMHC complexes are recognized by the T-cell receptors (TCRs) of CD8+ cytotoxic T lymphocytes (PubMed: 16339535). This recognition triggers T-cell activation, leading to the release of cytotoxic granules that induce apoptosis in the infected cell (StatPearls: NBK541071). In clinical settings, particularly in transplant recipients, CMV reactivation is a major cause of morbidity due to suppressed T-cell immunity (NIH: PMC7107425). Therapeutic interventions leverage these complexes by using adoptive T-cell therapy, such as Posoleucel, where CMV-specific T cells are infused into patients to provide antiviral protection (AlloVir, 2023). Additionally, novel approaches like TCR-engineered T cells are being developed to target specific CMV-pMHC combinations, such as those involving the HLA-A*02:01 allele (PubMed: 31515463). Monitoring the expression of these complexes and the corresponding T-cell response is vital for managing CMV-related complications in immunocompromised populations (PubMed: 25605914).
T-cell receptor (TCR) mediated recognition and subsequent activation of cytotoxic T lymphocytes (CTLs) to induce apoptosis in CMV-infected cells (PubMed: 16339535).
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