Immunoneutralization of IL-25 exaggerated DNBS-induced colitis in the IL-22-/- mice and ablated the anti-colitic effect of infection with H. diminta. Thus, while immune events in the early response to infection with H. diminuta are delayed in IL-22-/- mice (as is worm expulsion), the compensatory enhancement of IL-25 (and other immunoregulatory elements (e.g. IL-10)) provide resistance to colitis and also promote the anti-colitic effect driven as a consequence of the response to infection with H. diminuta. The data confirm the complex role of IL-22 in intestinal immunity. This evidence concerns the gene IL22 and colitis.