Epstein-Barr virus-derived peptide antigens presented by HLA-A11:01 (EBV-HLA-A11:01)

Epstein-Barr virus (EBV)-derived peptide antigens presented by the Human Leukocyte Antigen (HLA)-A11:01 allele are specific molecular complexes found on the surface of EBV-infected malignant cells (Tsao et al., 2014, Cancer Letters). These complexes consist of short viral protein fragments, typically derived from latent cycle proteins like LMP1, LMP2, or EBNA, bound within the groove of the HLA-A11:01 MHC class I molecule (Meij et al., 2002, Journal of Virology). This target is particularly significant in the context of nasopharyngeal carcinoma (NPC) and certain lymphomas, as the HLA-A11:01 allele is highly frequent in populations where these cancers are endemic, such as in Southeast Asia (Cho et al., 2018, Frontiers in Immunology). Therapeutic intervention involves the use of EBV-specific T-cell therapies or TCR-engineered T cells that are programmed to recognize these specific peptide-MHC combinations (Prockop et al., 2020, JCI). Upon binding, these therapeutic T cells trigger a cytotoxic response, leading to the selective destruction of the tumor cells. The high specificity of this interaction minimizes damage to healthy cells that do not express the viral antigens, though challenges such as HLA downregulation and the immunosuppressive tumor microenvironment remain (Hislop et al., 2007, Annual Review of Immunology).

Other names

EBV-A11:01 complexHLA-A*11:01 restricted EBV antigensEBV peptide-MHC class I complexEpstein-Barr virus-specific HLA-A11:01 restricted epitopes

Recognition of specific viral peptide-MHC complexes (e.g., LMP2 or EBNA3B peptides bound to HLA-A11:01) by the T-cell receptor (TCR) of therapeutic T cells, which triggers the release of perforin and granzymes, leading to apoptosis of the EBV-positive tumor cell (Cho et al., 2018, Frontiers in Immunology).