T cell-specific ablation of the stress kinase GCN2 results in the failure to resolve acute neuroinflammation in a mouse model of multiple sclerosis

Ablation of GCN2 in T cells does not impact the induction of experimental autoimmune encephalomyelitis in mice

The failure to resolve neuroinflammation in mice with GCN2 ablation in T cells is associated with a reduced influx of regulatory T cells

GCN2-deficient regulatory T cells display reduced migratory capacity to a chemokine gradient