IL2 and Autoimmunity: Indeed, the lethal autoimmunity observed in those mice are attributed to IL-2 signaling defect in Tregs, which constitutively express high-affinity IL-2R and utilize IL-2 as a survival factor.[3] Moreover, studies by our group and others have shown that Tregs exert their suppressive function at least partially through consuming IL-2, which creates an IL-2-deprivative environment to limit Teff cell expansion.[29]