The progression of Multiple sclerosis (MS) is marked by pathogenic degeneration and inflammation within the central nervous system (CNS). Whilst current therapies can modulate and limit inflammation for relapsing forms of MS, they do not address the need to restore function to damaged neural sites. Adult stem cells (SCs) have recently emerged as a novel therapeutic approach for a range of diseases, including MS, due to their innate immunomodulatory, neuro-protective and regenerative capabilities. However, there is a major limitation to these approaches in that therapeutic stem cells have poor penetration into the damaged CNS where they would exert these functions. To address this, we modified stem cells to express chemokine receptors known to be involved in the homing of lymphocytes to the CNS. In particular, overexpression of CCR6 enhances the migration of modified stem cells to CCL20 in-vitro. Furthermore, this modification led to the significant trafficking of stem cells into the inflamed CNS in experimental autoimmune encephalomyelitis (EAE), a model of MS. This enhanced infiltration into the inflamed CNS correlated with significantly delayed disease onset, and reduction in T cell entry into the CNS. The specific mechanism underlying the reduction in T cell infiltration after treatment with CCR6 expressing stem cells is currently under investigation.