Hepatitis B virus-induced lipid alterations contribute to natural killer T cell-dependent protective immunity.
Ontology highlight
ABSTRACT: In most adult humans, hepatitis B is a self-limiting disease leading to life-long protective immunity, which is the consequence of a robust adaptive immune response occurring weeks after hepatitis B virus (HBV) infection. Notably, HBV-specific T cells can be detected shortly after infection, but the mechanisms underlying this early immune priming and its consequences for subsequent control of viral replication are poorly understood. Using primary human and mouse hepatocytes and mouse models of transgenic and adenoviral HBV expression, we show that HBV-expressing hepatocytes produce endoplasmic reticulum (ER)-associated endogenous antigenic lipids including lysophospholipids that are generated by HBV-induced secretory phospholipases and that lead to activation of natural killer T (NKT) cell
SUBMITTER: Zeissig S
PROVIDER: S-EPMC3478098 | biostudies-literature | 2012 Jul
REPOSITORIES: biostudies-literature
ACCESS DATA