guest ::
| Home > Publications database > General control non-derepressible 2 (GCN2) in T cells controls disease progression of autoimmune neuroinflammation. |
| Home > Publications database > General control non-derepressible 2 (GCN2) in T cells controls disease progression of autoimmune neuroinflammation. |
| Journal Article | DKFZ-2017-04892 |
; ; ; ; ; ; ; ; ;
2016
Elsevier Science
Amsterdam [u.a.]
This record in other databases: 
Please use a persistent id in citations: 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.
Keyword(s): Annexin A5 ; Cytokines ; Myelin-Oligodendrocyte Glycoprotein ; Peptide Fragments ; myelin oligodendrocyte glycoprotein (35-55) ; Eif2ak4 protein, mouse ; Protein-Serine-Threonine Kinases
; BIOSIS Previews ; Current Contents - Life Sciences ; Ebsco Academic Search ; IF < 5 ; JCR ; NCBI Molecular Biology Database ; Nationallizenz
; SCOPUS ; Science Citation Index ; Science Citation Index Expanded ; Thomson Reuters Master Journal List ; Web of Science Core Collection
|
The record appears in these collections: |
