Crohn’s disease (CD) is a chronic relapsing, destructive inflammatory disease of the gastrointestinal (GI) tract, the cause of which remains still unknown. Accumulating evidence suggests that CD results from the imbalance between pro- and anti-inflammatory agents and the overactivity of T helper (Th)1. It seems that major cause of GI inflammation is an IL-12-driven Th1 response, which results in the generation of IFN-γ, the key inflammatory mediator. Recently, however, much attention has also been given to the possible involvement of Th17 cells in the pathogenesis of CD. This mini-review is aimed to summarize the current knowledge on the dual role of Th17 cells in CD.