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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, Vol. 297, 15.08.2016, p. 117-26.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Keil, M, Sonner, JK, Lanz, TV, Oezen, I, Bunse, T, Bittner, S, Meyer, HV, Meuth, SG, Wick, W & Platten, M 2016, 'General control non-derepressible 2 (GCN2) in T cells controls disease progression of autoimmune neuroinflammation', J NEUROIMMUNOL, vol. 297, pp. 117-26. https://doi.org/10.1016/j.jneuroim.2016.05.014

APA

Keil, M., Sonner, J. K., Lanz, T. V., Oezen, I., Bunse, T., Bittner, S., Meyer, H. V., Meuth, S. G., Wick, W., & Platten, M. (2016). General control non-derepressible 2 (GCN2) in T cells controls disease progression of autoimmune neuroinflammation. J NEUROIMMUNOL, 297, 117-26. https://doi.org/10.1016/j.jneuroim.2016.05.014

Vancouver

Keil M, Sonner JK, Lanz TV, Oezen I, Bunse T, Bittner S et al. General control non-derepressible 2 (GCN2) in T cells controls disease progression of autoimmune neuroinflammation. J NEUROIMMUNOL. 2016 Aug 15;297:117-26. https://doi.org/10.1016/j.jneuroim.2016.05.014

Bibtex

@article{2ed425e120314cca8c1f5a9046798a78,
title = "General control non-derepressible 2 (GCN2) in T cells controls disease progression of autoimmune neuroinflammation",
abstract = "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.",
keywords = "Animals, Annexin A5/metabolism, Astrocytes/metabolism, Brain/cytology, Cell Movement/physiology, Cytokines/metabolism, Disease Models, Animal, Disease Progression, Encephalomyelitis, Autoimmune, Experimental/immunology, Endothelial Cells/physiology, Female, Flow Cytometry, Male, Mice, Mice, Inbred C57BL, Mice, Transgenic, Myelin-Oligodendrocyte Glycoprotein/toxicity, Peptide Fragments/toxicity, Protein-Serine-Threonine Kinases/genetics, Statistics, Nonparametric, T-Lymphocytes, Regulatory/drug effects, Time Factors",
author = "Melanie Keil and Sonner, {Jana K} and Lanz, {Tobias V} and Iris Oezen and Theresa Bunse and Stefan Bittner and Meyer, {Hannah V} and Meuth, {Sven G} and Wolfgang Wick and Michael Platten",
note = "Copyright {\textcopyright} 2016. Published by Elsevier B.V.",
year = "2016",
month = aug,
day = "15",
doi = "10.1016/j.jneuroim.2016.05.014",
language = "English",
volume = "297",
pages = "117--26",
journal = "J NEUROIMMUNOL",
issn = "0165-5728",
publisher = "Elsevier",

}

RIS

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 -