The classical assumption indicates that helminth infections or helminth-derived molecules induce a type 2 immune response together with an immuno-regulatory response (including increase of IL-10, TGF-β, and CD4 + CD25 + FoxP3 + Treg cells) together with Th2-mediated tissue repair [34,35] that may counteract the Th1/Th17-mediated inflammatory effect observed in IBD. This evidence concerns the gene FOXP3 and helminthiasis.