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The protein encoded by IL25 is a cytokine that shares sequence similarity with interleukin 17. Additionally we are shipping IL25 Antibodies (268) and IL25 Proteins (58) and many more products for this protein.
Showing 10 out of 68 products:
Human IL25 ELISA Kit for Sandwich ELISA - ABIN414794
Javan, Seyfizadeh, Aslani, Farhoodi, Babaloo: Molecular analysis of interleukin-25 exons 1 and 2 and its serum levels in Iranian patients with multiple sclerosis. in American journal of clinical and experimental immunology 2014
Show all 4 Pubmed References
Human IL25 ELISA Kit for Sandwich ELISA - ABIN2703183
Wang, Fan, Lv, Yao, Wang, Huang, Meng, Fang, Lee, Corrigan, An, Ying: Interleukin-25 promotes basic fibroblast growth factor expression by human endothelial cells through interaction with IL-17RB, but not IL-17RA. in Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology 2013
Human IL25 ELISA Kit for Sandwich ELISA - ABIN365233
Hams, Armstrong, Barlow, Saunders, Schwartz, Cooke, Fahy, Crotty, Hirani, Flynn, Voehringer, McKenzie, Donnelly, Fallon: IL-25 and type 2 innate lymphoid cells induce pulmonary fibrosis. in Proceedings of the National Academy of Sciences of the United States of America 2014
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.
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.
Nasal Il-25 is overexpressed in patients with chronic rhinosinusitis with nasal polyps and airway hypersensitiveness.
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.
IL-25-induced activation of nasal fibroblast and its association with the remodeling of chronic rhinosinusitis with nasal polyposis
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).
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.
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.
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.
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.
these data suggest that IL-25 plays an inhibitory role in the growth and development of colonic tumors.
this study shows that the signaling axis of microRNA-31/interleukin-25 regulates Th1 (show HAND1 ELISA Kits)/Th17-mediated inflammation response in colitis
IL-25 is a component of the immune response that is regulated by a healthy microbiota and reduces pathology associated with Clostridium difficile Infection.
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
IL-17E (IL-25) and IL-17RB promote respiratory syncytial virus-induced pulmonary disease
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
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
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)
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.
The protein encoded by this gene is a cytokine that shares sequence similarity with interleukin 17. This cytokine can induce NF-kappaB activation, and stimulate the production of interleukin 8. Both this cytokine and interleukin 17B are ligands for the cytokine receptor IL17BR. Studies of a similar gene in mice suggest that this cytokine may be a pro-inflammatory cytokine favoring the Th2-type immune response. Alternative splicing results in multiple transcript variants.
, interleukin 17E
, interleukin 25
, interleukin 25-like