Interleukin 25 (IL25) ELISA Kits

Human Interleukin 25 (IL25) interaction partners

1. Endometrial stromal cells differentiate into decidual stromal cells in the presence of ovarian hormones, resulting in the upregulation of IL25/IL17RB (show IL17RB ELISA Kits) expression in endometrial stromal cells.

2. In conclusion, the findings of the present study suggest that IL-25 but not IL-33 (show IL33 ELISA Kits) might contribute to the pathogenesis of chronic eosinophilic inflammation of the lung in patients with CEP.

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

4. IL-4 (show IL4 ELISA Kits) 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.

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

6. The authors concluded that IL-25 provides protection from amebiasis, which is dependent upon intestinal eosinophils and suppression of TNF-alpha (show TNF ELISA Kits).

7. 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.

8. 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.

9. Chronic rhinosinusitis with nasal polyps (CRSwNP) epithelial cells release TSLP (show TSLP ELISA Kits) 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.

10. Increased induction and expression of TSLP (show TSLP ELISA Kits), IL-25, and IL-33 (show IL33 ELISA Kits) from nasal epithelial cells contribute to the pathophysiology of eosinophilic chronic rhinosinusitis.

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 (show HAND1 ELISA Kits)/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 (show IL33 ELISA Kits) and TSLP (show TSLP ELISA Kits) 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 (show PTPN11 ELISA Kits) 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 (show ICOS ELISA Kits) 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 (show IL33 ELISA Kits), IL-25 and TSLP (show TSLP ELISA Kits)

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.