Multiple sclerosis (MS) is regarded as a Tcell mediated autoimmune disease of the central nervous system (CNS). It has been traditionally seen as a Th1-mediated autoimmune disease, a notion which has been largely supported by studies in its animal model, experimental autoimmune encephalomyelitis (EAE). However, evidence has accumulated in recent years that a newly described lineage of (autoantigen-specific) T-cells, which are characterized by the production of the inflammatory cytokine interleukin 17 (Th17) cells, might be the relevant effector cell population instead. This is supported by studies both in MS patients and in the EAE mouse model. Research in this field currently centres on the endogenous factors which are required for the priming and expansion of CNS autoantigen specific Th17 cells as well as on exogenous factors which trigger Th17 differentiation and activation. This review tries to provide an overview of the relevant literature and to summarize the current body of evidence on the role of Th17 cells in CNS autoimmune disease.