Establishment of nematode infection despite increased Th2 responses and immunopathology after selective depletion of Foxp3+ cells.

Here, we show that Treg limit intestinal pathology during nematode infection and that they control the onset and magnitude of the anti-parasitic Th Th2 response. Using mice expressing the diphtheria toxin receptor under the control of the foxp3 locus, we removed Foxp3(+) Treg during the early phase of infection with Heligmosomoides polygyrus bakeri. Depletion of Treg in infected animals did not affect adult worm burden, but led to increased pathology at the site of infection.