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this study shows that IL-25 reduces Th17 cells and inflammatory responses in human peripheral blood mononuclear cells
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Endometrial stromal cells differentiate into decidual stromal cells in the presence of ovarian hormones, resulting in the upregulation of IL25/IL17RB expression in endometrial stromal cells.
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In conclusion, the findings of the present study suggest that IL-25 but not IL-33 might contribute to the pathogenesis of chronic eosinophilic inflammation of the lung in patients with CEP.
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Nasal Il-25 is overexpressed in patients with chronic rhinosinusitis with nasal polyps and airway hypersensitiveness.
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IL-4 signaling up-regulates the IL-25 axis in human monocytic cells, and IL-25 may provide autocrine signals in monocytes and macrophages to sustain IL-17Rb expression and predispose to alternative activation.
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IL-25-induced activation of nasal fibroblast and its association with the remodeling of chronic rhinosinusitis with nasal polyposis
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The authors concluded that IL-25 provides protection from amebiasis, which is dependent upon intestinal eosinophils and suppression of TNF-alpha.
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Inhibition of IL-25 resulted in decreased type 2 T cells and macrophages in the primary tumor microenvironments, both reported to enhance breast tumor invasion and subsequent metastasis to the lung.
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Our findings suggest that the IL-25/IL-25R axis may play an important role in promoting the recruitment and proinflammatory function of eosinophils in allergic asthma.
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Chronic rhinosinusitis with nasal polyps (CRSwNP) epithelial cells release TSLP and IL-25 when stimulated by poly(I:C) but not by DP or AF, suggesting that viral infection may contribute to maintain and amplify the T2 immune response seen in CRSwNP.
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Increased induction and expression of TSLP, IL-25, and IL-33 from nasal epithelial cells contribute to the pathophysiology of eosinophilic chronic rhinosinusitis.
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Women with endometriosis showed significantly higher levels of IL-25 in their PF (p=0.019) compared to controls. IL-25 levels did not correlate with the stage of endometriosis.
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IL-8 and IL-25 are targets of miR-20b.
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Our findings indicate that the alarmin cytokines IL-33 and IL-25 increase basophil activation and migratory potential, and may pose as a novel therapeutic targets for the treatment of allergic asthma.
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The IL17E rs79877597 SNP was a modifier of the risk for psoriasis disease severity and psoriatic arthritis.
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Findings indicate that the release of interleukin 25 (IL-25) from tumour-associated fibroblasts (TAFs) may serve as a check point for control of mammary tumour metastasis.
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Therefore, IL-17E/IL-17RB signaling represents a potential therapeutic target for treatment of hepatocellular carcinoma
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IL-25 upregulated PD-L1 surface expression through the signaling pathways of JNK and STAT3, with STAT3 found to constitutively occupy the proximal region of the PD-L1 promoter.
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we have demonstrated that the expression of ET-1 and IL-25 was coordinately upregulated in the lesional keratinocytes of patients with AD and a murine AD model.
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IL-25 overexpression was observed in eosinophilic chronic rhinosinusitis and may serve as a mediator of eosinophilic CRS.
