Fig 10. Proposed model of immune response upon H. diminuta infection in mice lacking IL-22.

The presence of H. diminuta provokes an increase in TH2 and regulatory populations both locally (small intestine) and systemically (MLN and spleen), which ultimately leads to worm expulsion in a non-permissive host (mouse). This regulatory network is responsible for blocking DNBS-colitis. Herein, we identified a heightened regulatory circuit in H. diminuta infected mice lacking IL-22.