In patients with chronic hepatitis B virus (HBV) and hepatitis C virus (HCV) infections, antiviral functions of T cells are impaired; these might be increased by blocking T-cell co-inhibitory pathways, such as preventing interaction between the receptor programmed death (PD)-1 and its ligand, PD-L1. We attempted to optimize the restoration of T-cell functions in patients with chronic HBV or HCV infection with a combination of reagents that block PD-1 interaction with PD-L1 and stimulate T-cell signaling via CD137, a member of the tumor necrosis factor-receptor family.
Combined blockade of programmed death-1 and activation of CD137 increase responses of human liver T cells against HBV, but not HCV / Fisicaro, Paola; Valdatta, Caterina; Massari, Marco; Loggi, Elisabetta; Ravanetti, Lara; Urbani, Simona; Giuberti, Tiziana; Cavalli, Albertina; Vandelli, Carmen; Andreone, Pietro; Missale, Gabriele; Ferrari, Carlo. - In: GASTROENTEROLOGY. - ISSN 0016-5085. - ELETTRONICO. - 143:6(2012), pp. 1576-1585.e4. [10.1053/j.gastro.2012.08.041]
Combined blockade of programmed death-1 and activation of CD137 increase responses of human liver T cells against HBV, but not HCV
VANDELLI, Carmen;Andreone, Pietro;
2012
Abstract
In patients with chronic hepatitis B virus (HBV) and hepatitis C virus (HCV) infections, antiviral functions of T cells are impaired; these might be increased by blocking T-cell co-inhibitory pathways, such as preventing interaction between the receptor programmed death (PD)-1 and its ligand, PD-L1. We attempted to optimize the restoration of T-cell functions in patients with chronic HBV or HCV infection with a combination of reagents that block PD-1 interaction with PD-L1 and stimulate T-cell signaling via CD137, a member of the tumor necrosis factor-receptor family.Pubblicazioni consigliate
I metadati presenti in IRIS UNIMORE sono rilasciati con licenza Creative Commons CC0 1.0 Universal, mentre i file delle pubblicazioni sono rilasciati con licenza Attribuzione 4.0 Internazionale (CC BY 4.0), salvo diversa indicazione.
In caso di violazione di copyright, contattare Supporto Iris