Updated project metadata. Previous studies of our group have shown that IL-25 is essential for the resistance to E. caproni infections and the susceptibility of mice relies on the inability of this host species to produce IL-25 in response to infection (14-15). Susceptibility of mice to primary E. caproni infection was associated with low levels of intestinal IL-25 expression, whilst deworming via administration of praziquantel (pzq) was accompanied by a steady increase in IL-25 expression and, in turn, by the onset of a Th2-type response that prevented the establishment of secondary infections (14-15). Although these facts, little is known about the mechanism by which IL-25 generates resistance against intestinal helminths. In the present work, we analyze the changes in the production of proteins induced by IL-25 in the ileum of mice that may be involved in the generation of resistance against intestinal helminths.