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impact of IL-6 on the Th9/Th17 balance depending on the predominant cytokine milieu; data suggest that the IL-6-mediated reduction of Th2-related IL-4 leads to a decline of the Th9 immune response and allows Th17 differentiation
the results of this study indicate that environmental cues dictate the instability of the Th9 phenotype, and they suggest approaches to enhance Th9 activity in beneficial immune responses
The germinal center development of memory B cells is promoted by follicular helpter T cell-derived IL-9.
In mice, the absence of IL-9 impaired ILC2 proliferation and activation of regulatory T (Treg) cells, and resulted in chronic arthritis with excessive cartilage destruction and bone loss.
These data indicate that IL-9 is an essential regulator of megakaryopoiesis and a promising therapeutic agent for treatment of thrombocytopenia such as CIT (show CIT Proteins).
Findings indicate that interleukin-17 (IL-17 (show IL17A Proteins)) inhibits the formation of malignant pleural effusion (MPE) and improves the survival of MPE via an interleukin-9 (IL-9)-dependent mechanism.
Group 2 innate lymphoid cells utilize the IRF4 (show IRF4 Proteins)-IL-9 module to coordinate epithelial cell maintenance of lung homeostasis.
Our results suggest that The Th9/IL-9 is involved in the pathogenesis of UC.
IL-9 exerted pro-atherosclerotic effects in ApoE (show APOE Proteins)-/- mice at least partially by inducing VCAM-1 (show VCAM1 Proteins) expression, which mediated inflammatory cell infiltration into atherosclerotic lesions.
IL-9 is dispensable for mucosal mast cell development but is necessary for their effective expansion to promote intestinal mastocytosis and susceptibility to experimental food allergy in an IL-9-dependent autocrine manner.
In vitro data indicate that IL9 is regulated by STAT3 (show STAT3 Proteins)/5 and in vivo results highlight the pro-neoplastic effect of IL9 on lymphoma T cells. The results suggest that IL9 and its regulators are promising new targets for therapy development in mycosis fungoides.
recent findings suggest that blockade of IL-9 signaling is effective in treating experimental models of autoimmune and chronic inflammatory diseases such as inflammatory bowel diseases, allergic disorders such as food allergy and asthma.
Findings showed that serum levels of IL-9 were elevated in diffuse large-B-cell lymphoma (DLBCL) patients and positive expression of IL-9 was correlated with adverse prognosis indicators. It directly effected proliferation and apoptosis of DLBCL cells by enhancing the expression of p21CIP1 (show CDKN1A Proteins) genes and promoted tumor cells to display resistance to chemotherapeutic drugs.
no differences were found in serum levels of IL-9 between different clinical forms of periportal fibrosis in human Schistosoma mansoni infection in Brazil
PU.1 and IL-9 may play a role in AD pathogenesis and relate to disease severity and clinical eruption types.
Inflammatory cell expression of IL-9 and IL-17C (show IL17C Proteins) were increased in chronic rhinosinusitis, particularly with allergy and asthma. These interleukins may contribute to the pathogenesis of chronic rhinosinusitis with nasal polyps as well as atopy and may serve as therapeutic targets for disease management
serum levels determined of both T cell polarizing (IL- 33 (show IL33 Proteins) and IL-12 (show IL12A Proteins)) and T cell effector (IFN-gamma (show IFNG Proteins), IL-4 (show IL4 Proteins), IL-10 (show IL10 Proteins), IL-17 (show IL17A Proteins) and IL-9) cytokines in T1DM (type-1 Diabetes Mellitus) subjects with and without microvascular complications (MVC). All the tested cytokines were significantly elevated in T1DM subjects except for IFN-gamma (show IFNG Proteins) with no significant difference between those with and without MVC.
results suggest that Th9 cells and IL-9 could play an important role in the pathogenesis of systemic sclerosis by modulating adaptive and innate immune responses and the production of autoantibodies and indicate the IL-9 pathway as a possible therapeutic target
TL1A (show TNFSF15 Proteins) differentially induces expression of TH17 effector cytokines IL-17 (show IL17A Proteins), -9, and -22 and provides a potential target for therapeutic intervention in TH17-driven chronic inflammatory diseases.
The protein encoded by this gene is a cytokine that acts as a regulator of a variety of hematopoietic cells. This cytokine stimulates cell proliferation and prevents apoptosis. It functions through the interleukin 9 receptor (IL9R), which activates different signal transducer and activator (STAT) proteins and thus connects this cytokine to various biological processes. The gene encoding this cytokine has been identified as a candidate gene for asthma. Genetic studies on a mouse model of asthma demonstrated that this cytokine is a determining factor in the pathogenesis of bronchial hyperresponsiveness.
, T-cell growth factor P40
, cytokine P40
, T-cell growth factor p40
, homolog of mouse T cell and mast cell growth factor 40
, p40 T-cell and mast cell growth factor
, p40 cytokine