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

Lang, Karl S. and Georgiev, Panco and Recher, Mike and Navarini, Alexander A. and Bergthaler, Andreas and Heikenwalder, Mathias and Harris, Nicola L. and Junt, Tobias and Odermatt, Bernhard and Clavien, Pierre-Alain and Pircher, Hanspeter and Akira, Shizuo and Hengartner, Hans and Zinkernagel, Rolf M.. (2006) Immunoprivileged status of the liver is controlled by Toll-like receptor 3 signaling. Journal of Clinical Investigation, 116 (9). pp. 2456-2463.

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Official URL: https://edoc.unibas.ch/76691/

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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-alpha and TNF-alpha 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.
Faculties and Departments:03 Faculty of Medicine > Bereich Spezialf├Ącher (Klinik) > Dermatologie USB > Dermatologie (Navarini)
03 Faculty of Medicine > Departement Klinische Forschung > Bereich Spezialf├Ącher (Klinik) > Dermatologie USB > Dermatologie (Navarini)
UniBasel Contributors:Navarini, Alexander
Item Type:Article, refereed
Article Subtype:Research Article
Publisher:American Society for Clinical Investigation
ISSN:0021-9738
e-ISSN:1558-8238
Note:Publication type according to Uni Basel Research Database: Journal article
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Last Modified:30 Sep 2020 11:10
Deposited On:30 Sep 2020 11:10

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