The understanding of the intricate mechanisms by which gut immune cells interact with each other and the intestinal flora is constantly developing. The mucosal immune system must retain the ability to mount a prompt response to intestinal pathogens while maintaining tolerance for commensal organisms. Effector T lymphocytes drive inflammation, whereas their actions are counteracted by populations of regulatory T cells (Treg), which act as an endogenous suppressor of mucosal inflammation. There is growing evidence that a loss of this delicate counterbalance is important in the etiology of inflammatory bowel disease (IBD). Here, we review studies highlighting alterations in Treg in the pathogenesis of IBD. Observations of dynamic changes in Treg activity with successful IBD treatment have highlighted their functional importance and potential to also serve as a biomarker of disease activity and to predict response to therapy. Furthermore, we explore the potential for adoptive transfer of Treg as part of IBD treatment.