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

Keil, M., Sonner, J. K., Lanz, T. V., Oezen, I., Bunse, T., Bittner, S., Meyer, H. V., Meuth, S. G., Wick, W., Platten, M. (August 2016) General control non-derepressible 2 (GCN2) in T cells controls disease progression of autoimmune neuroinflammation. J Neuroimmunol, 297. pp. 117-26. ISSN 0165-5728

URL: https://www.ncbi.nlm.nih.gov/pubmed/27397084
DOI: 10.1016/j.jneuroim.2016.05.014

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.

Item Type: Paper
Subjects: diseases & disorders > inflammation
CSHL Authors:
Communities: CSHL labs > Meyer Lab
Depositing User: Matthew Dunn
Date: 15 August 2016
Date Deposited: 25 Mar 2019 14:29
Last Modified: 25 Mar 2019 14:29
Related URLs:
URI: http://repository.cshl.edu/id/eprint/37740

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