ArticleParasites & vectors2020
Interleukin-25-mediated resistance against intestinal trematodes does not depend on the generation of Th2 responses.
Article in Parasites & vectors, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Proteomic reprogramming of ileal epithelial cells during homologous superimposed intestinal trematode infection reveals coordinated restoration of intestinal homeostasis.PLoS neglected tropical diseases · 2026Article
- Susceptibility of mice to primaryFrontiers in immunology · 2026Article
- Concomitant immunity against superimposed homologous Echinostoma caproni infections in mice is mediated by interleuquin-25.Memorias do Instituto Oswaldo Cruz · 2025Article
- Echinostomes and Other Intestinal Trematode Infections.Advances in experimental medicine and biology · 2024Review
- Changes in resident microbiota associated with mice susceptibility or resistance to the intestinal trematodeParasitology · 2022Article
- Neglected food-borne trematodiases: echinostomiasis and gastrodiscoidiasis.Parasitology · 2022Review
- Interleukin 25 and its biological features and function in intestinal diseases.Central-European journal of immunology · 2022Review
- Enteric Tuft Cells in Host-Parasite Interactions.Pathogens (Basel, Switzerland) · 2021Review
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Authors and funding
5 authors.
Funding
Abstract
backgroundThe cytokine interleukin-25 (IL-25) is recognized as the most relevant initiator of protective T helper 2 (Th2) responses in intestinal helminth infections. This cytokine induces resistance against several species of intestinal helminths, including the trematode Echinostoma caproni. E. caproni 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 E. caproni.
methodsThe factors that determine the production of IL-25 in mice experimentally infected with E. caproni were determined, as were the consequences of IL-25 production in terms of polarization of the immune response and resistance to infection.
resultsOur 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 E. caproni 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.
conclusionsIn 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.
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