We provide evidence that either 40% or 90% of deletion of the IL-4 receptor specifically within the Foxp3+ Treg cell population leads to aggravated tissue inflammation during helminth infections (Sm and N. brasiliensis [Nb] infections) and that this occurs as a result of a weakened Foxp3+ Treg cell compartment paralleled by an uncontrolled effector T-cell compartment. Here, FOXP3 is linked to infection.