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Citations to this article

Immunoprivileged status of the liver is controlled by Toll-like receptor 3 signaling
Karl S. Lang, … , Hans Hengartner, Rolf M. Zinkernagel
Karl S. Lang, … , Hans Hengartner, Rolf M. Zinkernagel
Published September 1, 2006
Citation Information: J Clin Invest. 2006;116(9):2456-2463. https://doi.org/10.1172/JCI28349.
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Research Article Autoimmunity Article has an altmetric score of 11

Immunoprivileged status of the liver is controlled by Toll-like receptor 3 signaling

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Abstract

The liver is known to be a classical immunoprivileged site with a relatively high resistance against immune responses. Here we demonstrate that highly activated liver-specific effector CD8+ T cells alone were not sufficient to trigger immune destruction of the liver in mice. Only additional innate immune signals orchestrated by TLR3 provoked liver damage. While TLR3 activation did not directly alter liver-specific CD8+ T cell function, it induced IFN-α and TNF-α release. These cytokines generated expression of the chemokine CXCL9 in the liver, thereby enhancing CD8+ T cell infiltration and liver disease in mice. Thus, nonspecific activation of innate immunity can drastically enhance susceptibility to immune destruction of a solid organ.

Authors

Karl S. Lang, Panco Georgiev, Mike Recher, Alexander A. Navarini, Andreas Bergthaler, Mathias Heikenwalder, Nicola L. Harris, Tobias Junt, Bernhard Odermatt, Pierre-Alain Clavien, Hanspeter Pircher, Shizuo Akira, Hans Hengartner, Rolf M. Zinkernagel

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Year: 2025 2024 2023 2022 2021 2020 2019 2018 2017 2016 2015 2014 2013 2012 2011 2010 2009 2008 2007 2006 Total
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