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• W2891021325 abstract "T cells play a crucial role in viral clearance and vaccine responses; however, the mechanisms that regulate their homeostasis during viral infections remain unclear. In this study, we investigated the machineries of T-cell homeostasis and telomeric DNA damage using a human model of hepatitis C virus (HCV) infection. We found that naïve CD4 T cells in chronically HCV-infected patients (HCV T cells) were significantly reduced due to apoptosis compared with age-matched healthy subjects (HSs). These HCV T cells were not only senescent, as demonstrated by overexpression of aging markers and particularly shortened telomeres; but also DNA damaged, as evidenced by increased dysfunctional telomere-induced foci (TIF). Mechanistically, the telomere shelterin protein, in particular telomeric repeat binding factor 2 (TRF2) that functions to protect telomeres from DNA damage, was significantly inhibited posttranscriptionally via the p53-dependent Siah-1a ubiquitination. Importantly, knockdown of TRF2 in healthy T cells resulted in increases in telomeric DNA damage and T-cell apoptosis, whereas overexpression of TRF2 in HCV T cells alleviated telomeric DNA damage and T-cell apoptosis. To the best of our knowledge, this is the first report revealing that inhibition of TRF2 promotes T-cell telomere attrition and telomeric DNA damage that accelerates T-cell senescent and apoptotic programs, which contribute to naïve T-cell loss during viral infection. Thus, restoring the impaired T-cell telomeric shelterin machinery may offer a new strategy to improve immunotherapy and vaccine response against human viral diseases." @default.
• W2891021325 created "2018-09-27" @default.
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• W2891021325 date "2018-09-05" @default.
• W2891021325 modified "2023-10-16" @default.
• W2891021325 title "Inhibition of TRF2 accelerates telomere attrition and DNA damage in naïve CD4 T cells during HCV infection" @default.
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• W2891021325 doi "https://doi.org/10.1038/s41419-018-0897-y" @default.
• W2891021325 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6125360" @default.
• W2891021325 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30185784" @default.
• W2891021325 hasPublicationYear "2018" @default.
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