The functionality of CCR6+ Th17 cells was demonstrated in adoptively transferred experimental autoimmune encephalomyelitis (at-EAE); transfer of lymph node cells containing CCR6+ Th17 cells led to severe disease while depletion of CCR6+ Th cells attenuated the course of at-EAE. The gene discussed is CCR6; the disease is experimental autoimmune encephalomyelitis.