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The Epstein–Barr virus (EBV) antigen–Human leukocyte antigen (HLA) complex is a molecular target formed by the presentation of EBV-derived peptides on the surface of infected cells via HLA molecules (Wikipedia, 2024). These peptides originate from latent viral proteins such as Latent Membrane Proteins (LMP1, LMP2) and Epstein-Barr Nuclear Antigens (EBNA1, EBNA3), which are expressed in various EBV-associated malignancies including post-transplant lymphoproliferative disorder (PTLD), nasopharyngeal carcinoma, and certain lymphomas (NIH, 2024). The complex is specifically recognized by the T-cell receptors (TCRs) of cytotoxic T lymphocytes, making it a critical focal point for cellular immunotherapy (Patsnap, 2024). Drugs like tabelecleucel (Ebvallo) utilize allogeneic EBV-specific T cells that bind to these complexes to induce apoptosis in malignant cells while minimizing damage to healthy tissue (NIH, 2024). Therapeutic challenges include the potential for immune evasion through HLA downregulation and the need for HLA matching between donor-derived cells and the patient (ASH Publications, 2019).
Adoptive T-cell therapy mediated by T-cell receptor (TCR) recognition of viral peptides presented on HLA molecules, leading to targeted lysis of EBV-infected cells.
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