Abstract
Virus-specific cytotoxic T Lymphocytes (CTLs) are crucial for the elimination of viral infections. So far, CTL-mediated killing of virus infected target cells is believed to depend on cell-cell contact depended recognition of antigen presented on MHC class I molecules. Therefore, the mechanisms determining the efficiency of target cell killing have been mainly investigated in an immune-centric fashion. Previous work on the non-canonical CTL effector function in our group shows selective killing of virus-infected hepatocytes by secreted TNF independent of direct target/effector cell contact. Therefore, we aimed to investigate the role of the target cells in antiviral immunity during experimental adenovirus infection as well as in HBV infection.
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