Taken together, our results showed that reprogrammed or conditioned recipient T cells, which produce IL-4 and TGF-β, are not only critical for the TGF-β–dependent expansion of donor Tregs (18) but also for the regulation of GVHD, filling an important gap in understanding our model, in which helminths induce T cell–intrinsic Th2 and TGF-β circuitries to suppress graft-versus-host reactivity. This evidence concerns the gene TGFB1 and graft versus host disease.