TY  - JOUR
AU  - Keil, Melanie
AU  - Sonner, Jana
AU  - Lanz, Tobias
AU  - Oezen, Iris
AU  - Bunse, Theresa
AU  - Bittner, Stefan
AU  - Meyer, Hannah V
AU  - Meuth, Sven G
AU  - Wick, Wolfgang
AU  - Platten, Michael
TI  - General control non-derepressible 2 (GCN2) in T cells controls disease progression of autoimmune neuroinflammation.
JO  - Journal of neuroimmunology
VL  - 297
SN  - 0165-5728
CY  - Amsterdam [u.a.]
PB  - Elsevier Science
M1  - DKFZ-2017-04892
SP  - 117 - 126
PY  - 2016
AB  - Relapsing-remitting multiple sclerosis (MS)(2) is characterized by phases of acute neuroinflammation followed by spontaneous remission. Termination of inflammation is accompanied by an influx of regulatory T cells (Tregs).(3) 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),(4) 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.
KW  - Annexin A5 (NLM Chemicals)
KW  - Cytokines (NLM Chemicals)
KW  - Myelin-Oligodendrocyte Glycoprotein (NLM Chemicals)
KW  - Peptide Fragments (NLM Chemicals)
KW  - myelin oligodendrocyte glycoprotein (35-55) (NLM Chemicals)
KW  - Eif2ak4 protein, mouse (NLM Chemicals)
KW  - Protein-Serine-Threonine Kinases (NLM Chemicals)
LB  - PUB:(DE-HGF)16
C6  - pmid:27397084
DO  - DOI:10.1016/j.jneuroim.2016.05.014
UR  - https://inrepo02.dkfz.de/record/128879
ER  -