ArticleParasites & vectors2026
ST2 blockade modulates IL-33-driven immune responses and is associated with reduced hepatic fibrosis in alveolar echinococcosis.
Article in Parasites & vectors, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- IL-33/ST2 Signaling Sustains Hepato-Intestinal Homeostasis by Orchestrating Vascular Surveillance and Immune Regulatory Circuits During Experimental Trypanosoma cruzi Infection.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
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Abstract
backgroundInfection with Echinococcus multilocularis causes alveolar echinococcosis (AE), a severe parasitic disease characterised by progressive hepatic infiltration and fibrosis. Current treatment options remain limited, and the immune-mediated mechanisms underlying fibrosis are not fully understood. This study investigated the role of the IL-33/ST2 axis in AE-associated immunopathology and evaluated the effects of ST2 blockade in an experimental model.
methodsA murine model of AE was established in C57BL/6 mice, which were allocated to untreated infected, anti-ST2-treated infected and uninfected control groups. Liver pathology and fibrosis were assessed using haematoxylin and eosin staining, Masson's trichrome staining and transmission electron microscopy. Immune and fibrotic markers were analysed by immunohistochemistry and immunofluorescence. In parallel, liver samples from patients with AE were examined to evaluate translational relevance. Systemic cytokine profiles were quantified to assess immune modulation.
resultsAnalysis of human AE liver samples showed an increased expression of IL-33/ST2 and associated immune and fibrotic markers, consistent with findings in the experimental mouse model. In infected mice, ST2 blockade significantly reduced metacestode lesion size and hepatic tissue invasion. This was accompanied by reduced fibrosis, as indicated by lower expression of α-smooth muscle actin, collagen I, matrix metalloproteinase-9 and tissue inhibitor of metalloproteinases-1. Anti-ST2 treatment was also associated with reduced hepatic infiltration of CD4⁺ T cells, B cells and M2 macrophages, along with decreased systemic levels of IFN-γ, TNF-α, IL-4, IL-13, IL-17 and IL-1β.
conclusionsST2 blockade reduced metacestode growth and was associated with attenuated hepatic inflammation and fibrosis, supporting a role for IL-33/ST2 signalling in AE progression. Given the concurrent reduction in parasite burden, further studies are needed to determine whether the anti-fibrotic effects of ST2 inhibition are independent of parasite control.
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