The hypothesis of helper T (T(h))1/T(h)2 cytokine balance was often invoked to explain the development of inflammatory diseases, including inflammatory bowel diseases (IBD). Recently, a newly identified class of regulatory T cells (Tregs), which suppress inflammation and helper T(Th)17 cells, which produce Th17 family cytokines has been recognized as an essential subpopulation in the development of almost all kinds of human and animal inflammatory diseases. T cell subsets can act as terminally differentiated lineages, but they have been increasingly noted to demonstrated plasticity, depending on their surrounding such as intestinal microbiota. Th17 cells and Th1 cells coordinate to play a critical role in the formation of inflammatory bowel diseases. We showed Th1 and Th17 cells are competitive in lymphopenic mice, and that their orchestration results in a merged clinical phenotype of the two types of murine colitis. We also showed that Th17 and Th17/Th1 cells become colitogenic alternative Th1 cells via Th17, Th17/Th1, and Th1-like cells, independently of classical Th1 cells. Treg cells suppress this pathway, resulting in accumulation of Th17 and Th17/Th1 cells. Here we review T cell development including their plasticity and recent advances in the study of such Treg cells and Th17 cells in the pathogenesis of IBD.