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This cytokine induces resistance against several species of intestinal helminths, including the trematode\n                      <jats:italic>Echinostoma caproni<\/jats:italic>\n                      .\n                      <jats:italic>E. caproni<\/jats:italic>\n                      has been extensively used as an experimental model to study the factors determining resistance to intestinal infections. In the study reported here, we assessed the role of IL-25 in the generation of resistance in mice infected with\n                      <jats:italic>E. caproni<\/jats:italic>\n                      .\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      The factors that determine the production of IL-25 in mice experimentally infected with\n                      <jats:italic>E. caproni<\/jats:italic>\n                      were determined, as were the consequences of IL-25 production in terms of polarization of the immune response and resistance to infection.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Our results show that the role of IL-25 in the polarization of the immune response differs between the primary and secondary immune responses. IL-25 is required for the development of a Th2 phenotype in primary\n                      <jats:italic>E. caproni<\/jats:italic>\n                      infections, but it can also promote the differentiation to Th2 memory cell subsets that enhance type-2 immunity in memory responses. However, the development of Th2 responses does not induce resistance to infection. The Th2 phenotype does not elicit resistance, and IL-25 is responsible for the resistance regardless of its type-2 cytokine activity and activation of signal transducer and activator of transcription (STAT6). Alternative activation of macrophages induced by IL-25 can be implicated in the resistance to infection.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>In contrast to primary infection, secondary infection elicits a type-2 immune response even in the absence of IL-25 expression. Despite the development of a type-2 response, mice are susceptible to secondary infection associated with the lack of IL-25. Resistance to infection is due to the production of IL-25, which acts autonomously from Th2 response in terms of parasite clearance.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Graphical Abstract<\/jats:title>\n                  <\/jats:sec>","DOI":"10.1186\/s13071-020-04467-7","type":"journal-article","created":{"date-parts":[[2020,12,4]],"date-time":"2020-12-04T06:03:33Z","timestamp":1607061813000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["Interleukin-25-mediated resistance against intestinal trematodes does not depend on the generation of Th2 responses"],"prefix":"10.1186","volume":"13","author":[{"given":"Mar\u00eda","family":"\u00c1lvarez-Izquierdo","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Miguel","family":"P\u00e9rez-Crespo","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J. 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