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- W2229811452 abstract "CD8(+) T cells specific to caspase-cleaved antigens derived from apoptotic T cells represent a principal player in chronic immune activation. Here, we found that both apoptotic epitope-specific and hepatitis C virus (HCV)-specific CD8(+) T cells were mostly confined within the effector memory (EM) or terminally differentiated EM CD45RA(+) cell subsets expressing a dysfunctional T-helper 1-like signature program in chronic HCV infection. However, apoptotic epitope-specific CD8(+) T cells produced tumor necrosis factor α and interleukin 2 at the intrahepatic level significantly more than HCV-specific CD8(+) T cells, despite both populations expressing high levels of programmed death 1 receptor. Contextually, only apoptotic epitope-specific CD8(+) T cells correlated with both interferon-stimulated gene levels in T cells and hepatic fibrosis score. Together, these data suggest that, compared with HCV-specific CD8(+) T cells, apoptotic epitope-specific CD8(+) T cells can better sustain chronic immune activation, owing to their capacity to produce tumor necrosis factor α, and exhibit greater resistance to inhibitory signals during chronic HCV infection." @default.
- W2229811452 created "2016-06-24" @default.
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- W2229811452 date "2015-09-19" @default.
- W2229811452 modified "2023-10-18" @default.
- W2229811452 title "Apoptotic Epitope–Specific CD8<sup>+</sup>T Cells and Interferon Signaling Intersect in Chronic Hepatitis C Virus Infection" @default.
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- W2229811452 doi "https://doi.org/10.1093/infdis/jiv460" @default.
- W2229811452 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26386427" @default.
- W2229811452 hasPublicationYear "2015" @default.
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