General control non-derepressible 2 (GCN2) in T cells controls disease progression of autoimmune neuroinflammation

Relapsing-remitting multiple sclerosis (MS)22MS: multiple sclerosis. is characterized by phases of acute neuroinflammation followed by spontaneous remission. Termination of inflammation is accompanied by an influx of regulatory T cells (Tregs).33Tregs: regulatory T cells. The molecular mechanisms re...

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Hauptverfasser: Keil, Melanie (VerfasserIn) , Lanz, Tobias (VerfasserIn) , Wick, Wolfgang (VerfasserIn) , Platten, Michael (VerfasserIn)
Dokumenttyp: Article (Journal)
Sprache:Englisch
Veröffentlicht: 20 May 2016
In: Journal of neuroimmunology
Year: 2016, Jahrgang: 297, Pages: 117-126
ISSN:1872-8421
DOI:10.1016/j.jneuroim.2016.05.014
Online-Zugang:Verlag, Volltext: http://dx.doi.org/10.1016/j.jneuroim.2016.05.014
Verlag, Volltext: http://www.sciencedirect.com/science/article/pii/S0165572816301199
Volltext
Verfasserangaben:Melanie Keil, Jana K. Sonner, Tobias V. Lanz, Iris Oezen, Theresa Bunse, Stefan Bittner, Hannah V. Meyer, Sven G. Meuth, Wolfgang Wick, Michael Platten

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520 |a Relapsing-remitting multiple sclerosis (MS)22MS: multiple sclerosis. is characterized by phases of acute neuroinflammation followed by spontaneous remission. Termination of inflammation is accompanied by an influx of regulatory T cells (Tregs).33Tregs: regulatory T cells. The molecular mechanisms responsible for directing Tregs into the inflamed CNS tissue, however, are incompletely understood. In an MS mouse model we show that the stress kinase general control non-derepressible 2 (GCN2),44GCN2: general control non-derepressible 2. expressed in T cells, contributes to the resolution of autoimmune neuroinflammation. Failure to recover from acute inflammation was associated with reduced frequencies of CNS-infiltrating Tregs. GCN2 deficient Tregs displayed impaired migration to a CCL2 gradient. These data suggest an important contribution of the T cell stress response to the resolution of autoimmune neuroinflammation. 
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