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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| Main Authors: | , , , |
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| Format: | Article (Journal) |
| Language: | English |
| Published: |
20 May 2016
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| In: |
Journal of neuroimmunology
Year: 2016, Volume: 297, Pages: 117-126 |
| ISSN: | 1872-8421 |
| DOI: | 10.1016/j.jneuroim.2016.05.014 |
| Online Access: | Verlag, Volltext: http://dx.doi.org/10.1016/j.jneuroim.2016.05.014 Verlag, Volltext: http://www.sciencedirect.com/science/article/pii/S0165572816301199 
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| Author Notes: | Melanie Keil, Jana K. Sonner, Tobias V. Lanz, Iris Oezen, Theresa Bunse, Stefan Bittner, Hannah V. Meyer, Sven G. Meuth, Wolfgang Wick, Michael Platten |
| Summary: | 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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| Item Description: | Gesehen am 21.03.2018 |
| Physical Description: | Online Resource |
| ISSN: | 1872-8421 |
| DOI: | 10.1016/j.jneuroim.2016.05.014 |