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The protein encoded by IL25 is a cytokine that shares sequence similarity with interleukin 17. Zusätzlich bieten wir Ihnen IL25 Antikörper (260) und IL25 Proteine (60) und viele weitere Produktgruppen zu diesem Protein an.
Showing 10 out of 69 products:
Human IL25 ELISA Kit für 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
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Human IL25 ELISA Kit für 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
Human IL25 ELISA Kit für 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
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 (zeige 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 (zeige IL33 ELISA Kits) and TSLP (zeige 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 (zeige 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 (zeige 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
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.
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 (zeige IL33 ELISA Kits), IL-25 and TSLP (zeige 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.
Nasal Il-25 is overexpressed in patients with chronic rhinosinusitis with nasal polyps and airway hypersensitiveness.
IL-4 (zeige 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 (zeige TNF ELISA Kits).
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 (zeige 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 (zeige TSLP ELISA Kits), IL-25, and IL-33 (zeige IL33 ELISA Kits) from nasal epithelial cells contribute to the pathophysiology of eosinophilic chronic rhinosinusitis.
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.
IL-8 (zeige IL8 ELISA Kits) and IL-25 are targets of miR (zeige MLXIP ELISA Kits)-20b.
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 25-like
, UPF0556 protein C19orf10 homolog
, interleukin 17E