| http://purl.uniprot.org/citations/25218666 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/25218666 | http://www.w3.org/2000/01/rdf-schema#comment | "Background and objectiveAcute rejection is still a major cause of graft dysfunction and would jeopardize recipients' post-transplantation survival. Current studies demonstrate that Galectin-9 (Gal-9) is associated with down-regulation of pro-inflammatory cytokines, thus, possesses a negative immune regulatory role. However, the specific role of Gal-9 in liver transplant remains unknown.MethodsTo establish acute rejection models of rat liver transplantation (Lewis-BN, n = 45), recipients were randomly divided into following three groups: the transfected group (n = 15); the blank plasmid group (n = 15); and the control group (n = 15). The transfected group was perfused with Ad-galectin-9 through the portal vein during the cold ischemia period. The blank plasmid group was perfused with non-target vector, and the control group was perfused with saline. The acute rejection was assayed by pathological examination; Gal-9, T-bet, RORγt, GATA3 and Foxp3 mRNA expression was detected by real-time PCR; Western blots and enzyme-linked immunosorbent assays were performed to measure IFN-γ, IL-10 and IL-17 expression.ResultsThe pathological change of the transfected group was ameliorated than that of the other two groups. The Gal-9 mRNA level in the transfected group was much higher than that in the other two groups (*P < 0.05); T-bet and RORγt mRNA levels were significantly lower in the transfected group than in the other two groups while GATA3 and Foxp3 were not shown statistics significances (*P < 0.05). The IFN-γ and IL-17 levels in the transfected group were significantly lower than in the other two groups (*P < 0.05 for both protein and serum levels).ConclusionUp-regulation of Gal-9 in vivo turns immune system toward immnuosuppression and prolongs rats liver allograft survival by the diminishment of Th1/Th17."xsd:string |
| http://purl.uniprot.org/citations/25218666 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.imlet.2014.09.002"xsd:string |
| http://purl.uniprot.org/citations/25218666 | http://purl.uniprot.org/core/author | "Chen Y."xsd:string |
| http://purl.uniprot.org/citations/25218666 | http://purl.uniprot.org/core/author | "Li J.Z."xsd:string |
| http://purl.uniprot.org/citations/25218666 | http://purl.uniprot.org/core/author | "Liu Y.M."xsd:string |
| http://purl.uniprot.org/citations/25218666 | http://purl.uniprot.org/core/author | "Gong J.P."xsd:string |
| http://purl.uniprot.org/citations/25218666 | http://purl.uniprot.org/core/date | "2014"xsd:gYear |
| http://purl.uniprot.org/citations/25218666 | http://purl.uniprot.org/core/name | "Immunol Lett"xsd:string |
| http://purl.uniprot.org/citations/25218666 | http://purl.uniprot.org/core/pages | "217-222"xsd:string |
| http://purl.uniprot.org/citations/25218666 | http://purl.uniprot.org/core/title | "Up-regulation of Galectin-9 in vivo results in immunosuppressive effects and prolongs survival of liver allograft in rats."xsd:string |
| http://purl.uniprot.org/citations/25218666 | http://purl.uniprot.org/core/volume | "162"xsd:string |
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