Specifically in the context of helminth parasitism, in murine infections with Brugia malayi[61], Heligmosomoides polygyrus[62], [63], [64] and Strongyloides ratti[65] all drive marked increases in Tregs, which in the latter two models can be shown to functionally inhibit the host Th2 protective response and promote chronic infection; moreover, blocking TGF-β signaling in H. polygyrus infection results in greater worm expulsion [66], establishing a mechanistic link to this key cytokine. Here, TGFB1 is linked to infection.