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Barili, Valeria; Fisicaro, Paola; Montanini, Barbara; Acerbi, Greta; Filippi, Anita; Forleo, Giovanna; Romualdi, Chiara; Ferracin, Manuela; Guerrieri, Francesca; Pedrazzi, Giuseppe; Boni, Carolina; Rossi, Marzia; Vecchi, Andrea; Penna, Amalia; Zecca, Alessandra; Mori, Cristina; Orlandini, Alessandra; Negri, Elisa; Pesci, Marco; Massari, Marco; Missale, Gabriele; Levrero, Massimo; Ottonello, Simone; Ferrari, Carlo
Nature communications, 01/2020, Letnik: 11, Številka: 1Journal Article
Hepatitis C virus infection (HCV) represents a unique model to characterize, from early to late stages of infection, the T cell differentiation process leading to exhaustion of human CD8+ T cells. Here we show that in early HCV infection, exhaustion-committed virus-specific CD8+ T cells display a marked upregulation of transcription associated with impaired glycolytic and mitochondrial functions, that are linked to enhanced ataxia-telangiectasia mutated (ATM) and p53 signaling. After evolution to chronic infection, exhaustion of HCV-specific T cell responses is instead characterized by a broad gene downregulation associated with a wide metabolic and anti-viral function impairment, which can be rescued by histone methyltransferase inhibitors. These results have implications not only for treatment of HCV-positive patients not responding to last-generation antivirals, but also for other chronic pathologies associated with T cell dysfunction, including cancer.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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Vir: Osebne bibliografije
in: SICRIS
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