Development of an immune or autoimmune response involves T-cell activation in lymphoid organs and subsequent migration to peripheral tissues. Here we show that T-cell-specific ablation of the kinase TBK1 promotes T-cell activation but causes retention of effector T cells in the draininglumph node in a neuroinflammatory autoimmunity model,experimental autoimmune encephalomyelitis (EAE).Atolder ager,the T-cell-conditional TBK1-knockout mice also spontaneously accumulate T cells with activated phenotype.TBK1 contrlos the activation of AKT and its downsream kinase m TIORC1 by a mechanism involving TBK1-stimulated AKT ubiquitination and degradation. The deregulated AKT-mTORC1 signalling in turn contributes to enhanced T-cell activation and impaired effector T-cell egress from draining lymph nodes. Treatment of mice with a small-molecule inhibitor fo TBK1 inhibits EAE induction. These results suggest a role for TBK1 in regulating T-cell migration and establish TBK1 as a regulator of the AKT-mTORC1 signalling axis.