Aliment Pharmacol Ther
October 2022
Background: Hepatitis B virus (HBV)-specific CD8 cell response restoration during nucleos(t)ide analogue (NUC) treatment could lead to off-treatment HBV control in e-antigen-negative chronic hepatitis B (CHBe(-)).
Aim: To predict this response with variables involved in T-cell exhaustion for use as a treatment stopping tool.
Methods: In NUC-treated CHBe(-) patients, we considered a functional response in cases with HBV-specific CD8 cells against core and polymerase HBV epitopes able to proliferate and secrete type I cytokines after antigen encounter.
Thirty to fifty percent of hepatocellular carcinomas (HCC) display an immune class genetic signature. In this type of tumor, HCC-specific CD8 T cells carry out a key role in HCC control. Those potential reactive HCC-specific CD8 T cells recognize either HCC immunogenic neoantigens or aberrantly expressed host's antigens, but they become progressively exhausted or deleted.
View Article and Find Full Text PDFHepatitis C virus (HCV)-specific CD8 T cell response is essential in natural HCV infection control, but it becomes exhausted during persistent infection. Nowadays, chronic HCV infection can be resolved by direct acting anti-viral treatment, but there are still some non-responders that could benefit from CD8 T cell response restoration. To become fully reactive, T cell needs the complete release of T cell receptor (TCR) signalling but, during exhaustion this is blocked by the PD-1 effect on CD28 triggering.
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