General control non-derepressible 2 (GCN2) in T cells controls disease progression of autoimmune neuroinflammation
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General control non-derepressible 2 (GCN2) in T cells controls disease progression of autoimmune neuroinflammation. / Keil, Melanie; Sonner, Jana K; Lanz, Tobias V; Oezen, Iris; Bunse, Theresa; Bittner, Stefan; Meyer, Hannah V; Meuth, Sven G; Wick, Wolfgang; Platten, Michael.
in: J NEUROIMMUNOL, Jahrgang 297, 15.08.2016, S. 117-26.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - General control non-derepressible 2 (GCN2) in T cells controls disease progression of autoimmune neuroinflammation
AU - Keil, Melanie
AU - Sonner, Jana K
AU - Lanz, Tobias V
AU - Oezen, Iris
AU - Bunse, Theresa
AU - Bittner, Stefan
AU - Meyer, Hannah V
AU - Meuth, Sven G
AU - Wick, Wolfgang
AU - Platten, Michael
N1 - Copyright © 2016. Published by Elsevier B.V.
PY - 2016/8/15
Y1 - 2016/8/15
N2 - 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.
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 - Animals
KW - Annexin A5/metabolism
KW - Astrocytes/metabolism
KW - Brain/cytology
KW - Cell Movement/physiology
KW - Cytokines/metabolism
KW - Disease Models, Animal
KW - Disease Progression
KW - Encephalomyelitis, Autoimmune, Experimental/immunology
KW - Endothelial Cells/physiology
KW - Female
KW - Flow Cytometry
KW - Male
KW - Mice
KW - Mice, Inbred C57BL
KW - Mice, Transgenic
KW - Myelin-Oligodendrocyte Glycoprotein/toxicity
KW - Peptide Fragments/toxicity
KW - Protein-Serine-Threonine Kinases/genetics
KW - Statistics, Nonparametric
KW - T-Lymphocytes, Regulatory/drug effects
KW - Time Factors
U2 - 10.1016/j.jneuroim.2016.05.014
DO - 10.1016/j.jneuroim.2016.05.014
M3 - SCORING: Journal article
C2 - 27397084
VL - 297
SP - 117
EP - 126
JO - J NEUROIMMUNOL
JF - J NEUROIMMUNOL
SN - 0165-5728
ER -