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these findings indicated that IL-9 facilitated platelet function through the JAK2/STAT3 pathway, thus promoting the development of deep venous thrombosis
Results indicated that interleukin 9 (IL-9) was an important type of cytokine involved in the progression of Schistosoma japonicum infection-induced hepatic damage.
IL9 CNS-25/IL9 CNS-18 is a critical and conserved regulatory element for IL-9 production in mice and humans.
Data show that interferon regulatory factor 1 (IRF1) occupancy correlates with decreased interferon regulatory factor 4 (IRF4) abundance, suggesting an IRF1-IRF4-binding competition at the interleukin 9 (Il9) locus.
Furthermore, chromatin immunoprecipitation (ChIP) followed by luciferase assays revealed direct binding of Foxo1 to both the Il9 and Irf4 promoters and induces their transactivation.
CXCL10, not CXCL9 or CXCL11, induced IL-9 expression in the liver tissue.
Chronic kidney disease aggravates vein graft disease through mechanisms involving IL-9 and mast cell activation.
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.
Findings indicate that interleukin-17 (IL-17) 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-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-/- mice at least partially by inducing VCAM-1 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.
IL-9 production following chlamydial lung infection is redundant for host defense against the intracellular bacteria
IL-25-stimulated dendritic cells rapidly induced mediators, such as the chemokine CCL17, which, in turn, attracted IL-9-producing T cells
Data show that the expression of interleukin-9 (IL-9) was higher, but interleukin-10 (IL-10) was lower in asthma group, and that Th9 cells might play an important role in the pathogenesis of asthma.
CD4+IL-9+ T cells were infiltrated in both the skin and muscle tissues in dermatomyositis (DM) patients with elevated serum IL-9 levels. Thus, IL-9 may play an important role in the development of DM.
this study shows that intensified IL-9 production is associated with the immunopathogenesis of active ulcerative colitis
Our study reveals that degeneration and destruction of cartilage may be related to the production of IL-9 in osteonecrosis of the femoral head patients. In a human primary chondrocytes culture model, IL-9 increased the degeneration of cartilage; blocking JAK-STAT signaling alleviated this effect.
Having one or more copies of the 1635A allele was associated with increased cytomegalovirus acquisition in HIV-infected infants (42 vs. 11%, P = 0.03) and increased risk of Epstein-Barr virus acquisition in HIV-exposed uninfected infants (hazard ratio = 4.2, P = 0.02) compared with 1635GG.
T Helper 9 cells may be the major source of interleukin-9 (IL-9) in children with allergic asthma. In these patients, IL-9 impairs interferon gamma production and synergistically promotes interleukin-4-induced IgE secretion.
Increased expression of nuclear factor of activated T cells 1 drives IL-9-mediated allergic asthma.
these results demonstrated that IL-9-expressing Th9 cells were upregulated in breast cancer patients and potentially possessed antitumor roles by enhancing CD8+ T cell-mediated cytotoxicity
Serum IL-9 and IL-22 are associated with eosinophilia in cow's milk allergy, and decrease in these two cytokines with occurs with cow's milk elimination.
The systemic IL9 level is higher in ulcerative colitis and corresponds with endoscopic inflammation, suggesting its possible application as a negative marker of mucosal healing.
These findings suggest that IL-9 is involved in the pathogenesis of VKH disease, and that IL-9 might also enhance the inflammatory response by increasing the secretion of IL-17, an established proinflammatory cytokine in VKH disease
Data suggest that the conditions defined for strong induction of interleukin-9 (IL-9) might be relevant for the development of Vdelta2 T-cell-based immunotherapy. IL-9 might be relevant for the development of Vdelta2 T-cell-based immunotherapy.
expression of IL-9, IFN-gamma and IL-22 was higher in CLP compared to that of OLP
An aberrant expression profile of Th9/IL-9 was associated with pathogenesis of immune thrombocytopenia, possibly through cooperative interaction with Th17/IL-17.
In vitro data indicate that IL9 is regulated by STAT3/5 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 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
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