Roberto Aiolfi

TL;DR: The unprecedented observation that antiplatelet therapy inhibits or delays immune-mediated hepatocarcinogenesis suggests that platelets may be key players in the pathogenesis of HBV-associated liver cancer and supports the notion that immune- mediated necroinflammatory reactions are an important cause of hepatocellular transformation during chronic hepatitis.

TL;DR: Advanced imaging in mouse models of hepatitis B virus pathogenesis is used to understand the mechanisms whereby effector CD8(+) T cells home to the liver, recognize antigens, and deploy effector functions and suggest how liver fibrosis might reduce CD8 TE immune surveillance toward infected or transformed hepatocytes.

TL;DR: It is demonstrated that KCs do not directly induce hepatocellular injury nor do they affect the pathogenic potential of virus-specific CD8 T cells, instead, KCs limit the severity of liver immunopathology.

TL;DR: This review discusses major platelet functions in immune and inflammatory responses, with an emphasis on recent pre-clinical studies that suggest that the inhibition of platelet activation pathways represent an alternative therapeutic strategy with potential use in the reduction of virus-specific T cell-mediated chronic inflammation, liver fibrosis and hepatocellular carcinoma in patients who are chronically infected with HBV.

TL;DR: It is reported that Cl 13 infection in multiple inbred mouse strains elicits opposite phenotypes: acute death in 7 to 9 d associated with a robust T cell response contrasted to suppression of T cellresponse leading to persistent infection with normal life span.