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
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: | https://repository.cshl.edu/id/eprint/37740 |
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