CD4 T helper 2 (Th2) cells, with the characteristic interleukin (IL)-4, IL-5, and IL-13 cytokine secretion profile, play an important role in the initiation and perpetuation of allergic airways disease. It is clear from recent studies that CD4+ T cells with distinct cytokine-producing abilities have regulatory functions that limit allergic inflammation. Studies of allergic airway inflammation in mice have identified different types of T regulatory cells (Tregs) that control the disease phenotype. The cytokines associated with the Treg phenotype in mice include both soluble and cell membrane-bound transforming growth factor (TGF)-beta and IL-10. Both contact-dependent mechanisms involving membrane-bound TGF-beta and contact-independent mechanisms involving soluble TGF-beta and IL-10 have been invoked to describe the function of these Tregs. In humans, studies of milk allergy show an association between circulating CD4+CD25+ Tregs and tolerance to the causative allergen, beta-lactoglobulin. The identification of Tregs as suppressors of allergic disease may promote the development of new therapeutic strategies.