A specific deficiency of CTLA‐4 in Treg cells results in spontaneous development of systemic lymphoproliferation, lethal T cell‐mediated autoimmune disease, and hyperproduction of IgE in mice.57 Since the balance between allergen‐specific Treg cells and Th2 seems to play a decisive role in the development of the immune response to allergens,58 we hypothesize that the production of Treg cell induced by the TGFβ1‐mim in Phl p 5‐sensitized mice suppressed Th2 polarization. This evidence concerns the gene CTLA4 and autoimmune disease.