We show that neither the IFN-γ–producing Th17 cell progeny (ex-Th17 and IL-17/IFN-γ double producers in the case of EAE, or ex-Th17 cells in the case of H. hepaticus colitis) nor long-term Th17 cell maintenance (in the case of EAE) is essential for the establishment of T cell–mediated immunopathology. Here, IL17A is linked to colitis.