Interleukin 25 (IL25) ELISA Kits

Human Interleukin 25 (IL25) interaction partners

1. The data demonstrate that an IL-17-induced autoregulatory circuit in keratinocytes is mediated by IL-25 and suggest that this circuit could be targeted in the treatment of psoriasis patients.

2. this review details the structural characteristics, expression patterns, responder cells, biological properties, and role of IL-25 in disease pathogenesis

3. this study shows that IL-25 reduces Th17 cells and inflammatory responses in human peripheral blood mononuclear cells

4. 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.

5. 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.

6. Nasal Il-25 is overexpressed in patients with chronic rhinosinusitis with nasal polyps and airway hypersensitiveness.

7. 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.

8. IL-25-induced activation of nasal fibroblast and its association with the remodeling of chronic rhinosinusitis with nasal polyposis

9. The authors concluded that IL-25 provides protection from amebiasis, which is dependent upon intestinal eosinophils and suppression of TNF-alpha.

10. 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.

11. 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.

12. 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.

13. Increased induction and expression of TSLP, IL-25, and IL-33 from nasal epithelial cells contribute to the pathophysiology of eosinophilic chronic rhinosinusitis.

14. 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.

15. IL-8 and IL-25 are targets of miR-20b.

16. 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.

17. The IL17E rs79877597 SNP was a modifier of the risk for psoriasis disease severity and psoriatic arthritis.

18. 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.

19. Therefore, IL-17E/IL-17RB signaling represents a potential therapeutic target for treatment of hepatocellular carcinoma

20. 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.

Mouse (Murine) Interleukin 25 (IL25) interaction partners

1. these data suggest that IL-25 plays an inhibitory role in the growth and development of colonic tumors.

2. this study shows that the signaling axis of microRNA-31/interleukin-25 regulates Th1/Th17-mediated inflammation response in colitis

3. IL-25 is a component of the immune response that is regulated by a healthy microbiota and reduces pathology associated with Clostridium difficile Infection.

4. study concludes that IL-33 and TSLP are required for epithelial cell IL-25 expression, mucous metaplasia, and ILC2 expansion following early-life rhinovirus infection

5. IL-17E (IL-25) and IL-17RB promote respiratory syncytial virus-induced pulmonary disease

6. data suggested that deletion of Shp2 impaired IL-25 production in bronchial epithelial cells in vitro, but might yet have minor influence on OVA-induced allergic reaction in vivo

7. study showed that IL-25 promoted the accumulation of ICOS and T1/ST2 on nuocytes, further induced the pro-inflammatory Th2 cells, and promoted Th2 cytokine responses in OVA-induced airway inflammation

8. 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.

9. this study shows that activation of primed TH2 cells occurs independently of group 2 innate lymphoid cells or their cytokines but that the effector function of both cell types was dependent on combinatorial exposure to IL-33, IL-25 and TSLP

10. These data demonstrate that IL-25 is critical for host protective immunity against H. polygyrus bakeri infection, highlighting its potential application as a therapeutic agent against parasitic nematode infection worldwide.

11. 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.

12. IL-25 and CD4(+) TH2 cells enhance type 2 innate lymphoid cell-derived IL-13 production, which promotes IgE-mediated experimental food allergy.

13. IL-22 restrains tapeworm-mediated protection against colitis via regulation of IL-25 expression

14. IL-25 promotes the function of CD4+CD25+ T regulatory cells and prolongs skin-graft survival in murine models

15. IL-25 and IL-33 are critical for induction of Th2-type cytokine-mediated allergic airway eosinophilia, but not Th17-type cytokine-mediated airway neutrophilia, at the local sites of lungs in the challenge phase of mice sensitized EC with OVA

16. Suggest that chronic exposure of murine airways to IL-25 alone is able to reproduce a local angiogenic milieu in asthmatic mice.

17. 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.

18. Colonic isolated lymphoid follicles develop in the absence of a number of factors required for the development of their small intestinal counterparts and can be specifically suppressed by factors other than IL-25.

19. These data demonstrate that dysregulated IL-25 expression contributes to lipid accumulation, whereas exogenous IL-25 protects against hepatic steatosis through IL-13 activation of STAT6.

20. Concerted activity of IgG1 antibodies and IL-4/IL-25-dependent effector cells trap helminth larvae in the tissues following vaccination with defined secreted antigens, providing sterile immunity to challenge infection.