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Cell Rep. 2012 Sep 27;2(3):478-87. doi: 10.1016/j.celrep.2012.08.001. Epub 2012 Aug 30.

TNF-induced target cell killing by CTL activated through cross-presentation.

Author information

1
Institutes of Molecular Medicine and Experimental Immunology, Universität Bonn, 53105 Bonn, Germany.

Abstract

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.

PMID:
22939982
DOI:
10.1016/j.celrep.2012.08.001
[Indexed for MEDLINE]
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