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• W2073281641 endingPage "2021" @default.
• W2073281641 startingPage "2007" @default.
• W2073281641 abstract "Objectives: Although CD8+ T cells play a critical role in the control of HIV-1 infection, their antiviral efficacy can be limited by antigenic variation and immune exhaustion. The latter phenomenon is characterized by the upregulation of multiple inhibitory receptors, such as programmed death-1 (PD-1), CD244 and lymphocyte activation gene-3 (LAG-3), which modulate the functional capabilities of CD8+ T cells. Design and methods: Here, we used an array of different human leukocyte antigen (HLA)-B*15 : 03 and HLA-B*42 : 01 tetramers to characterize inhibitory receptor expression as a function of differentiation on HIV-1-specific CD8+ T-cell populations (n = 128) spanning 11 different epitope targets. Results: Expression levels of PD-1, but not CD244 or LAG-3, varied substantially across epitope specificities both within and between individuals. Differential expression of PD-1 on T-cell receptor (TCR) clonotypes within individual HIV-1-specific CD8+ T-cell populations was also apparent, independent of clonal dominance hierarchies. Positive correlations were detected between PD-1 expression and plasma viral load, which were reinforced by stratification for epitope sequence stability and dictated by effector memory CD8+ T cells. Conclusion: Collectively, these data suggest that PD-1 expression on HIV-1-specific CD8+ T cells tracks antigen load at the level of epitope specificity and TCR clonotype usage. These findings are important because they provide evidence that PD-1 expression levels are influenced by peptide/HLA class I antigen exposure." @default.
• W2073281641 created "2016-06-24" @default.
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• W2073281641 creator A5089411837 @default.
• W2073281641 date "2014-09-10" @default.
• W2073281641 modified "2023-09-26" @default.
• W2073281641 title "Programmed death-1 expression on HIV-1-specific CD8+ T cells is shaped by epitope specificity, T-cell receptor clonotype usage and antigen load" @default.
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• W2073281641 doi "https://doi.org/10.1097/qad.0000000000000362" @default.
• W2073281641 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4166042" @default.
• W2073281641 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24906112" @default.
• W2073281641 hasPublicationYear "2014" @default.
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