Interleukin-17-secreting γδ T cells (γδT17 cells) are inflammatory innate-like immune cells that contribute to the pathogenesis of a number of autoimmune conditions. γδ T cell-deficient mice exhibit reduced symptoms of experimental autoimmune encephalomyelitis (EAE), the murine model of multiple sclerosis (MS). γδT17 cells are known to infiltrate the site of inflammation, the central nervous system (CNS), early during EAE pathogenesis. However, the mechanism by which this occurs is unknown. Migration of leukocytes is coordinated by chemokine receptors and their cognate chemokine ligands, which often act in a subset-specific manner to recruit them to the site of inflammation. Thus γδT17 cells were screened for chemokine receptor expression, and were found to co-express the inflammatory chemokine receptors CCR2 and CCR6. These receptors were shown to be functional by ex vivo chemotaxis assays, and were also expressed by skin- and mucosa-resident γδT17 cells. Both CCR2 and CCR6 are already implicated in EAE pathogenesis, driving macrophage and Th17 recruitment to the CNS, respectively. Indeed, γδT17 infiltration into the CNS during EAE onset was reduced in Ccr2-/-, Ccr6-/- and Ccr2-/-Ccr6-/-mice, suggesting an important role for these receptors in their recruitment. Mixed bone marrow chimaeras will be utilised to investigate if this trafficking defect is γδ T cell-intrinsic. As chemokine receptor antagonists have high therapeutic potential, establishing the trafficking requirements of γδT17 cells may present new targets for the treatment of human autoimmune conditions.