Auto-aggressive CXCR6+ CD8 T cells cause liver immune pathology in NASH

Abstract

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Initial Experience of Atezolizumab Plus Bevacizumab for Unresectable Hepatocellular Carcinoma in Real-World Clinical Practice

“…In the clinical trial, the frequency of liver damage was 20%. In atezolizumab plus bevacizumab, liver damage was thought to be caused by infiltration of activated T cell to the liver, especially in the patients with non-alcoholic steatohepatitis [18,19]. However, its mechanism is not fully understood.…”

Target Therapies for NASH/NAFLD: From the Molecular Aspect to the Pharmacological and Surgical Alternatives

“…Recent studies showed that liver inflammation, injury, and steatosis might be improved by inhibitors against this pathway [117][118][119][120]. The immune system has also been linked to NASH progression, in particular, an auto-aggression of CD8 T cells within the liver [121]. All these potential new pharmacological targets are based on the NAFLD/NASH pathogenesis, which is still under evaluation.…”

Lack of response to immunotherapy in non-alcoholic steatohepatitis related hepatocellular carcinoma

“…(1)] investigated the activation mechanism of the CD8 + cells in the NASH mouse model (5). They revealed that the unconventionally increased CD8 + T cells in the NASH mouse model are resident-like CXCR6 + CD8 + T cells.…”

“…• PD-1 antibody promotes HCC incidence through increased CD8 + PD-1 + T cell NASH, non-alcoholic steatohepatitis; PD-1, programmed cell death 1; HCC, hepatocellular carcinoma. (5).…”