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• W4280489411 endingPage "1019" @default.
• W4280489411 startingPage "1019" @default.
• W4280489411 abstract "HLA-B*57:01 is an HLA allelic variant associated with positive outcomes during viral infections through interactions with T cells and NK cells, but severe disease in persons treated with the anti-HIV-1 drug abacavir. The role of HLA-B*57:01 in the context of HSV infection is unknown. We identified an HLA-B*57:01-restricted CD8 T-cell epitope in the ICP22 (US1) protein of HSV-2. CD8 T cells reactive to the HSV-2 ICP22 epitope recognized the orthologous HSV-1 peptide, but not closely related peptides in human IFNL2 or IFNL3. Abacavir did not alter the CD8 T-cell recognition of the HSV or self-derived peptides. Unexpectedly, a tetramer of HSV-2 ICP22 epitope (228-236) and HLA-B*57:01 bound both CD8 T cells and NK cells. Tetramer specificity for KIR3DL1 was confirmed using KIR3DL1 overexpression on non-human primate cells lacking human KIR and studies with blocking anti-KIR3DL1 antibody. Interaction with KIR3DL1 was generalizable to donors lacking the HLA-B*57:01 genotype or HSV seropositivity. These findings suggest a mechanism for the recognition of HSV infection by NK cells or KIR-expressing T cells via KIR3DL1." @default.
• W4280489411 created "2022-05-22" @default.
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• W4280489411 date "2022-05-11" @default.
• W4280489411 modified "2023-10-01" @default.
• W4280489411 title "HLA-B*57:01 Complexed to a CD8 T-Cell Epitope from the HSV-2 ICP22 Protein Binds NK and T Cells through KIR3DL1" @default.
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• W4280489411 doi "https://doi.org/10.3390/v14051019" @default.
• W4280489411 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/35632760" @default.
• W4280489411 hasPublicationYear "2022" @default.
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