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http://purl.uniprot.org/citations/25786692http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/25786692http://www.w3.org/2000/01/rdf-schema#comment"The TNF family cytokine TL1A (Tnfsf15) costimulates T cells and type 2 innate lymphocytes (ILC2) through its receptor DR3 (Tnfrsf25). DR3-deficient mice have reduced T cell accumulation at the site of inflammation and reduced ILC2-dependent immune responses in a number of models of autoimmune and allergic diseases. In allergic lung disease models, immunopathology and local Th2 and ILC2 accumulation is reduced in DR3-deficient mice despite normal systemic priming of Th2 responses and generation of T cells secreting IL-13 and IL-4, prompting the question of whether TL1A promotes the development of other T cell subsets that secrete cytokines to drive allergic disease. In this study, we find that TL1A potently promotes generation of murine T cells producing IL-9 (Th9) by signaling through DR3 in a cell-intrinsic manner. TL1A enhances Th9 differentiation through an IL-2 and STAT5-dependent mechanism, unlike the TNF-family member OX40, which promotes Th9 through IL-4 and STAT6. Th9 differentiated in the presence of TL1A are more pathogenic, and endogenous TL1A signaling through DR3 on T cells is required for maximal pathology and IL-9 production in allergic lung inflammation. Taken together, these data identify TL1A-DR3 interactions as a novel pathway that promotes Th9 differentiation and pathogenicity. TL1A may be a potential therapeutic target in diseases dependent on IL-9."xsd:string
http://purl.uniprot.org/citations/25786692http://purl.org/dc/terms/identifier"doi:10.4049/jimmunol.1401220"xsd:string
http://purl.uniprot.org/citations/25786692http://purl.uniprot.org/core/author"Choi Y."xsd:string
http://purl.uniprot.org/citations/25786692http://purl.uniprot.org/core/author"Yang X.P."xsd:string
http://purl.uniprot.org/citations/25786692http://purl.uniprot.org/core/author"Siegel R.M."xsd:string
http://purl.uniprot.org/citations/25786692http://purl.uniprot.org/core/author"Kaplan M.H."xsd:string
http://purl.uniprot.org/citations/25786692http://purl.uniprot.org/core/author"Tan C."xsd:string
http://purl.uniprot.org/citations/25786692http://purl.uniprot.org/core/author"Goswami R."xsd:string
http://purl.uniprot.org/citations/25786692http://purl.uniprot.org/core/author"Walsh M."xsd:string
http://purl.uniprot.org/citations/25786692http://purl.uniprot.org/core/author"O'Shea J.J."xsd:string
http://purl.uniprot.org/citations/25786692http://purl.uniprot.org/core/author"Gomez-Rodriguez J."xsd:string
http://purl.uniprot.org/citations/25786692http://purl.uniprot.org/core/author"Pelletier M."xsd:string
http://purl.uniprot.org/citations/25786692http://purl.uniprot.org/core/author"Gery I."xsd:string
http://purl.uniprot.org/citations/25786692http://purl.uniprot.org/core/author"Meylan F."xsd:string
http://purl.uniprot.org/citations/25786692http://purl.uniprot.org/core/author"Cruz A.C."xsd:string
http://purl.uniprot.org/citations/25786692http://purl.uniprot.org/core/author"Richard A.C."xsd:string
http://purl.uniprot.org/citations/25786692http://purl.uniprot.org/core/author"Gabay O."xsd:string
http://purl.uniprot.org/citations/25786692http://purl.uniprot.org/core/author"Ferdinand J.R."xsd:string
http://purl.uniprot.org/citations/25786692http://purl.uniprot.org/core/author"Al-Shamkhani A."xsd:string
http://purl.uniprot.org/citations/25786692http://purl.uniprot.org/core/author"Keane-Myers A."xsd:string
http://purl.uniprot.org/citations/25786692http://purl.uniprot.org/core/author"Hayes E.T."xsd:string
http://purl.uniprot.org/citations/25786692http://purl.uniprot.org/core/author"Hawley E.T."xsd:string
http://purl.uniprot.org/citations/25786692http://purl.uniprot.org/core/author"Penumetcha P."xsd:string
http://purl.uniprot.org/citations/25786692http://purl.uniprot.org/core/date"2015"xsd:gYear