Unbalanced immune reactions against allergens are caused by Th2 cells, which are the basis of immunoglobulin E (IgE)-mediated symptoms of allergy and asthma. Although Th2 cells are essential for allergy, they are not sufficient to cause disease, because regulatory T cells (Tregs) control their activity and expansion. Therefore, Tregs are assumed to play an important role not only in the sensitization but also in established allergic disease under therapy. A key factor of Tregs is FOXP3, which, upon expression, is sufficient to induce regulatory T-cell phenotypes. The initiation and suppressive function of FOXP3 and Tregs in the context of allergic asthma are discussed in this review.