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http://purl.uniprot.org/citations/32889153http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/32889153http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/32889153http://www.w3.org/2000/01/rdf-schema#comment"Human basophils regulate allergic reactions by secreting histamine, interleukin 4 (IL-4) and IL-13 through key surface receptors FcεRI as well as IL-3R, which are constitutively expressed on basophils. IL-3/IL-3R signaling axis plays key roles in regulating the development and activation of basophils. We and others have shown that IL-3-induced surface receptors e.g. ST2, IL-17RB and IL-2 receptors regulate the biology of basophils. However, the expression and function of IL-3-induced surface proteins on human basophils remain to be elucidated. We in this study aimed to identify new basophil activation regulators by transcriptomic analysis of IL-3-stimulated basophils. Gene expression microarray analysis of IL-3-treated basophils revealed 2050 differentially expressed genes, of which 323 genes encoded surface proteins including GITR. We identified that GITR was preferentially induced by IL-3 rather than anti-IgE, IL-33, fMLP and C5a. IL-3-induced GITR was suppressed by inhibitors targeting JAK2, PI3K and MEK1/2. Stimulation of IL-3-treated basophils by GITR enhanced the expression of IL-4 and IL-13. Moreover, IgE-mediated degranulation was enhanced by GITRL in the presence of IL-3. This transcriptomic analysis of IL-3-activated basophils helps to identify novel activation regulator. IL-3-induced GITR promoted the activation of basophils, adding new evidence supporting GITR as an important player in Th2-associated immune responses."xsd:string
http://purl.uniprot.org/citations/32889153http://purl.org/dc/terms/identifier"doi:10.1016/j.cyto.2020.155268"xsd:string
http://purl.uniprot.org/citations/32889153http://purl.org/dc/terms/identifier"doi:10.1016/j.cyto.2020.155268"xsd:string
http://purl.uniprot.org/citations/32889153http://purl.uniprot.org/core/author"He C."xsd:string
http://purl.uniprot.org/citations/32889153http://purl.uniprot.org/core/author"He C."xsd:string
http://purl.uniprot.org/citations/32889153http://purl.uniprot.org/core/author"Hong L."xsd:string
http://purl.uniprot.org/citations/32889153http://purl.uniprot.org/core/author"Hong L."xsd:string
http://purl.uniprot.org/citations/32889153http://purl.uniprot.org/core/author"Gao S."xsd:string
http://purl.uniprot.org/citations/32889153http://purl.uniprot.org/core/author"Gao S."xsd:string
http://purl.uniprot.org/citations/32889153http://purl.uniprot.org/core/author"Shi Y."xsd:string
http://purl.uniprot.org/citations/32889153http://purl.uniprot.org/core/author"Shi Y."xsd:string
http://purl.uniprot.org/citations/32889153http://purl.uniprot.org/core/author"Pan S."xsd:string
http://purl.uniprot.org/citations/32889153http://purl.uniprot.org/core/author"Pan S."xsd:string
http://purl.uniprot.org/citations/32889153http://purl.uniprot.org/core/author"Tang Y."xsd:string
http://purl.uniprot.org/citations/32889153http://purl.uniprot.org/core/author"Tang Y."xsd:string
http://purl.uniprot.org/citations/32889153http://purl.uniprot.org/core/author"Xu M."xsd:string
http://purl.uniprot.org/citations/32889153http://purl.uniprot.org/core/author"Xu M."xsd:string
http://purl.uniprot.org/citations/32889153http://purl.uniprot.org/core/author"Wang Q."xsd:string
http://purl.uniprot.org/citations/32889153http://purl.uniprot.org/core/author"Wang Q."xsd:string
http://purl.uniprot.org/citations/32889153http://purl.uniprot.org/core/author"Shi Z."xsd:string
http://purl.uniprot.org/citations/32889153http://purl.uniprot.org/core/author"Shi Z."xsd:string
http://purl.uniprot.org/citations/32889153http://purl.uniprot.org/core/author"Wang H."xsd:string
http://purl.uniprot.org/citations/32889153http://purl.uniprot.org/core/author"Wang H."xsd:string