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http://purl.uniprot.org/citations/25941256http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/25941256http://www.w3.org/2000/01/rdf-schema#comment"Unconventional T cells such as γδ T cells, natural killer T cells (NKT cells) and mucosal-associated invariant T cells (MAIT cells) are a major component of the immune system; however, the cytokine signaling pathways that control their development and function in humans are unknown. Primary immunodeficiencies caused by single gene mutations provide a unique opportunity to investigate the role of specific molecules in regulating human lymphocyte development and function. We found that individuals with loss-of-function mutations in STAT3 had reduced numbers of peripheral blood MAIT and NKT but not γδ T cells. Analysis of STAT3 mosaic individuals revealed that this effect was cell intrinsic. Surprisingly, the residual STAT3-deficient MAIT cells expressed normal levels of the transcription factor RORγt. Despite this, they displayed a deficiency in secretion of IL-17A and IL-17F, but were able to secrete normal levels of cytokines such as IFNγ and TNF. The deficiency in MAIT and NKT cells in STAT3-deficient patients was mirrored by loss-of-function mutations in IL12RB1 and IL21R, respectively. Thus, these results reveal for the first time the essential role of STAT3 signaling downstream of IL-23R and IL-21R in controlling human MAIT and NKT cell numbers."xsd:string
http://purl.uniprot.org/citations/25941256http://purl.org/dc/terms/identifier"doi:10.1084/jem.20141992"xsd:string
http://purl.uniprot.org/citations/25941256http://purl.uniprot.org/core/author"Kobayashi M."xsd:string
http://purl.uniprot.org/citations/25941256http://purl.uniprot.org/core/author"Gray P."xsd:string
http://purl.uniprot.org/citations/25941256http://purl.uniprot.org/core/author"Holland S.M."xsd:string
http://purl.uniprot.org/citations/25941256http://purl.uniprot.org/core/author"Rao G."xsd:string
http://purl.uniprot.org/citations/25941256http://purl.uniprot.org/core/author"Rossjohn J."xsd:string
http://purl.uniprot.org/citations/25941256http://purl.uniprot.org/core/author"McCluskey J."xsd:string
http://purl.uniprot.org/citations/25941256http://purl.uniprot.org/core/author"Casanova J.L."xsd:string
http://purl.uniprot.org/citations/25941256http://purl.uniprot.org/core/author"Wong M."xsd:string
http://purl.uniprot.org/citations/25941256http://purl.uniprot.org/core/author"Freeman A.F."xsd:string
http://purl.uniprot.org/citations/25941256http://purl.uniprot.org/core/author"Payne K."xsd:string
http://purl.uniprot.org/citations/25941256http://purl.uniprot.org/core/author"Bustamante J."xsd:string
http://purl.uniprot.org/citations/25941256http://purl.uniprot.org/core/author"Warnatz K."xsd:string
http://purl.uniprot.org/citations/25941256http://purl.uniprot.org/core/author"Picard C."xsd:string
http://purl.uniprot.org/citations/25941256http://purl.uniprot.org/core/author"Uzel G."xsd:string
http://purl.uniprot.org/citations/25941256http://purl.uniprot.org/core/author"Boisson-Dupuis S."xsd:string
http://purl.uniprot.org/citations/25941256http://purl.uniprot.org/core/author"Ma C.S."xsd:string
http://purl.uniprot.org/citations/25941256http://purl.uniprot.org/core/author"Stepensky P."xsd:string
http://purl.uniprot.org/citations/25941256http://purl.uniprot.org/core/author"Tangye S.G."xsd:string
http://purl.uniprot.org/citations/25941256http://purl.uniprot.org/core/author"Lau A."xsd:string
http://purl.uniprot.org/citations/25941256http://purl.uniprot.org/core/author"Arkwright P.D."xsd:string
http://purl.uniprot.org/citations/25941256http://purl.uniprot.org/core/author"Deenick E.K."xsd:string
http://purl.uniprot.org/citations/25941256http://purl.uniprot.org/core/author"Peake J."xsd:string