edoc

Toll-like receptor engagement converts T-cell autoreactivity into overt autoimmune disease

Lang, Karl S. and Recher, Mike and Junt, Tobias and Navarini, Alexander A. and Harris, Nicola L. and Freigang, Stefan and Odermatt, Bernhard and Conrad, Curdin and Ittner, Lars M. and Bauer, Stefan and Luther, Sanjiv A. and Uematsu, Satoshi and Akira, Shizuo and Hengartner, Hans and Zinkernagel, Rolf M.. (2005) Toll-like receptor engagement converts T-cell autoreactivity into overt autoimmune disease. Nat Med, 11 (2). pp. 138-145.

Full text not available from this repository.

Official URL: https://edoc.unibas.ch/76695/

Downloads: Statistics Overview

Abstract

Autoimmune diabetes mellitus in humans is characterized by immunological destruction of pancreatic beta islet cells. We investigated the circumstances under which CD8(+) T cells specific for pancreatic beta-islet antigens induce disease in mice expressing lymphocytic choriomeningitis virus (LCMV) glycoprotein (GP) as a transgene under the control of the rat insulin promoter. In contrast to infection with LCMV, immunization with LCMV-GP derived peptide did not induce autoimmune diabetes despite large numbers of autoreactive cytotoxic T cells. Only subsequent treatment with Toll-like receptor ligands elicited overt autoimmune disease. This difference was critically regulated by the peripheral target organ itself, which upregulated class I major histocompatibility complex (MHC) in response to systemic Toll-like receptor-triggered interferon-alpha production. These data identify the 'inflammatory status' of the target organ as a separate and limiting factor determining the development of autoimmune disease.
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:Nature Publishing Company
ISSN:1078-8956
e-ISSN:1546-170X
Note:Publication type according to Uni Basel Research Database: Journal article
Identification Number:
Last Modified:30 Sep 2020 11:20
Deposited On:30 Sep 2020 11:20

Repository Staff Only: item control page