Alteration of the cytokine signature by various TLR ligands in different T cell populations in MOG37-50 and MOG35-55-induced EAE in C57BL/6 mice

Copyright © 2016 Elsevier Inc. All rights reserved.

Bibliographische Detailangaben
Veröffentlicht in:Clinical immunology (Orlando, Fla.). - 1999. - 170(2016) vom: 01. Sept., Seite 22-30
1. Verfasser: Steckner, Corinna (VerfasserIn)
Weitere Verfasser: Weber, Andreas, Mausberg, Anne K, Heininger, Maximilian, Opdenhövel, Felicitas, Kieseier, Bernd C, Hartung, Hans P, Hofstetter, Harald H
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2016
Zugriff auf das übergeordnete Werk:Clinical immunology (Orlando, Fla.)
Schlagworte:Journal Article Research Support, Non-U.S. Gov't EAE IL-17 MOG T cell TLR Cytokines Interleukin-17 Ligands mehr... Lipopolysaccharides Myelin-Oligodendrocyte Glycoprotein Peptide Fragments Toll-Like Receptors myelin oligodendrocyte glycoprotein (35-55) Guanosine 12133JR80S Interferon-gamma 82115-62-6 loxoribine 9CAS0V66OI
Beschreibung
Zusammenfassung:Copyright © 2016 Elsevier Inc. All rights reserved.
Interleukin 17 (IL-17), produced by T cells, plays an important role in Multiple Sclerosis (MS) and its animal model, Experimental Autoimmune Encephalomyelitis (EAE). In contrast to IL-17-producing CD4+ T cells, the contribution of IL-17-producing CD8+ T cells (Tc17) in CNS autoimmunity has been investigated less intensively. Here we investigate the role of TC17 in EAE. We compare different T cell populations and their cytokine pattern in the MOG35-55- and MOG37-50-induced EAE. We detected a similar cytokine phenotype for both EAE models in the autoimmune process assessed at different stages. Regarding the migratory activity, an involvement of IL-17 and IFN-γ in disease onset was suggested. Furthermore, we show that PAMPs have the ability to drive autoimmune process. To modify the cytokine pattern of different T cell populations, a combination of distinct factors is required (the activation of MyD88 or Syk, the genetic background, the presence of APCs and CD4+ T cells)
Beschreibung:Date Completed 30.03.2017
Date Revised 30.03.2017
published: Print-Electronic
Citation Status MEDLINE
ISSN:1521-7035
DOI:10.1016/j.clim.2016.05.008