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

• Verfasst von: Keil, Melanie [VerfasserIn]
• Verfasst von: Lanz, Tobias [VerfasserIn]
• Verfasst von: Wick, Wolfgang [VerfasserIn]
• Verfasst von: Platten, Michael [VerfasserIn]
• Titel: General control non-derepressible 2 (GCN2) in T cells controls disease progression of autoimmune neuroinflammation
• Verf.angabe: Melanie Keil, Jana K. Sonner, Tobias V. Lanz, Iris Oezen, Theresa Bunse, Stefan Bittner, Hannah V. Meyer, Sven G. Meuth, Wolfgang Wick, Michael Platten
• Umfang: 10 S.
• Fussnoten: Gesehen am 21.03.2018
• Titel Quelle: Enthalten in: Journal of neuroimmunology
• Jahr Quelle: 2016
• Band/Heft Quelle: 297(2016), S. 117-126
• ISSN Quelle: 1872-8421
• DOI: doi:10.1016/j.jneuroim.2016.05.014
• Datenträger: Online-Ressource
• Sprache: eng
• K10plus-PPN: 1571293779

Abstract

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.