作者: Giovanni Sitia , Matteo Iannacone , Roberto Aiolfi , Masanori Isogawa , Nico van Rooijen
DOI: 10.1371/JOURNAL.PPAT.1002061
关键词:
摘要: Kupffer cells (KCs) are widely considered important contributors to liver injury during viral hepatitis due their pro-inflammatory activity. Herein we utilized B virus (HBV)-replication competent transgenic mice and wild-type infected with a hepatotropic adenovirus demonstrate that KCs do not directly induce hepatocellular nor they affect the pathogenic potential of virus-specific CD8 T cells. Instead, limit severity immunopathology. Mechanistically, our results most compatible hypothesis contain immunopathology by removing apoptotic hepatocytes in manner largely dependent on scavenger receptors. Apoptotic readily removed become secondarily necrotic release high-mobility group box 1 (HMGB-1) protein, promoting organ infiltration inflammatory cells, particularly neutrophils. Overall, these indicate resolve rather than worsen