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TNF-induced target cell killing by CTL activated through cross-presentation.
Cell Rep. 2, 478-487 (2012)
Viruses can escape cytotoxic T cell (CTL) immunity by avoiding presentation of viral components via endogenous MHC class I antigen presentation in infected cells. Cross-priming of viral antigens circumvents such immune escape by allowing noninfected dendritic cells to activate virus-specific CTLs, but they remain ineffective against infected cells in which immune escape is functional. Here, we show that cross-presentation of antigen released from adenovirus-infected hepatocytes by liver sinusoidal endothelial cells stimulated cross-primed effector CTLs to release tumor necrosis factor (TNF), which killed virus-infected hepatocytes through caspase activation. TNF receptor signaling specifically eliminated infected hepatocytes that showed impaired anti-apoptotic defense. Thus, CTL immune surveillance against infection relies on two similarly important but distinct effector functions that are both MHC restricted, requiring either direct antigen recognition on target cells and canonical CTL effector function or cross-presentation and a noncanonical effector function mediated by TNF.
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
HEPATITIS-B-VIRUS; CD8(+) T-CELLS; ENDOTHELIAL-CELLS; EXOGENOUS ANTIGEN; DENDRITIC CELLS; IMMUNE-RESPONSE; LIVER-DAMAGE; MOUSE MODEL; INFECTIONS; TOLERANCE
ISSN (print) / ISBN
2211-1247
e-ISSN
2211-1247
Journal
Cell Reports
Quellenangaben
Volume: 2,
Issue: 3,
Pages: 478-487
Publisher
Cell Press
Non-patent literature
Publications
Reviewing status
Peer reviewed
Institute(s)
Institute of Virology (VIRO)