ArticleMemorias do Instituto Oswaldo Cruz2025
Concomitant immunity against superimposed homologous Echinostoma caproni infections in mice is mediated by interleuquin-25.
Article in Memorias do Instituto Oswaldo Cruz, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 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
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5 authors.
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Abstract
backgroundThe Institute of Cancer Research (ICR) mouse-Echinostoma caproni model is used to study mechanisms generating resistance against intestinal helminths due to the development chronic primary infections with Th1 responses, and partial resistance to secondary infections.
objectivesThis study aimed to evaluate the generation of concomitant immunity against superimposed homologous E. caproni infection.
methodsChanges in cytokine expression and macrophages markers as a consequence of primary infection, superimposed infection and superimposed infection in anti (α)-interleuquin(IL)-25-treated mice were investigated by real-time polymerase chain reaction (PCR). Translocation and phosphorylation of STAT6 were studied by indirect immunofluorescence (IIF) on intestinal tissue sections. The IIF technique was also used to label M1 and M2 macrophages to confirm the activation pathways.
findingsPrimary E. caproni infections elicit partial resistance against homologous superimposed infections. The animal groups displayed distinct patterns in the expression of cytokines, macrophages markers and IL-13Rα2 as well as STAT6 phosphorylation in a process mediated by IL-25. Resistance appears to rely on the ability of to induce IL-13Rα2 upregulation. MAIN
conclusionsThe concomitant immunity is based the production of IL-25, rather than in the development of Th2 responses. Regarding the IL-25-dependent mechanisms responsible for concomitant immunity, the ability of IL-25 to induce IL-13Rα2 upregulation which serves to limit the production of other regulatory proteins such as Ym1 affecting the maintenance of mucosal homeostasis appears to be critical.
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