Viral hepatitis and serotonin: altering cytotoxic T-lymphocyte function in the liver.
Evaluation of: Lang PA, Contaldo C, Georgiev P et al. Aggravation of viral hepatitis by platelet-derived serotonin. Nat. Med. 14(7), 756-761 (2008). The study of host-virus interactions that determine liver disease pathogenesis and outcome of infection have been key issues of interest in the field of viral hepatitis. It is generally accepted that infection with noncytopathic viruses, such as HBV and HCV, triggers the activation of immunological events involving virus-specific cytotoxic T lymphocytes (CTLs), which helps to control viral replication but at the same time causes liver inflammation and damage due to the recruitment of antigen-nonspecific inflammatory cells. However, not much is known regarding the factors modulating intrahepatic CTL function or the complex interactions in the liver microenvironment that leads to liver immunopathology. The paper under evaluation here introduces the concept that platelet-derived serotonin supports virus persistence in the liver and aggravates CTL-mediated liver immunopathology.
Koh
Sarene
S
Laboratory of Hepatic Viral Diseases, Singapore Institute for Clinical Sciences, A*STAR, Singapore. sarene.koh@ki.se
Bertoletti
Antonio
A