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http://purl.uniprot.org/citations/22387553http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/22387553http://www.w3.org/2000/01/rdf-schema#comment"We have investigated the mechanism underlying the immunoregulatory function of membrane Ig-like transcript 3 (ILT3) and soluble ILT3Fc. microRNA (miRNA) expression profile identified genes that were downregulated in ILT3-induced human CD8(+) T suppressor cells (Ts) while upregulated in T cells primed in the absence of ILT3. We found that miR-21, miR-30b, and miR-155 target the 3'-untranslated region of genes whose expression was strongly increased in ILT3Fc-induced Ts, such as dual specificity phosphatase 10, B cell CLL/lymphoma 6, and suppressor of cytokine signaling 1, respectively. Transfection of miRNA mimics or inhibitors and site-specific mutagenesis of their 3'-untranslated region binding sites indicated that B cell CLL/lymphoma 6, dual specificity phosphatase 10, and suppressor of cytokine signaling 1 are direct targets of miR-30b, miR-21, and miR-155. Primed CD8(+) T cells transfected with miR-21&30b, miR-21&155, or miR-21&30b&155 inhibitors displayed suppressor activity when added to autologous CD3-triggered CD4 T cells. Luciferase reporter assays of miR-21 and miR-155 indicated that their transcription is highly dependent on AP-1. Analysis of activated T cells showed that ILT3Fc inhibited the translocation to the nucleus of the AP-1 subunits, FOSB and c-FOS, and the phosphorylation of ZAP70 and phospholipase C-γ 1. In conclusion, ILT3Fc inhibits T cell activation and induces the generation of Ts targeting multiple inflammatory miRNA pathways."xsd:string
http://purl.uniprot.org/citations/22387553http://purl.org/dc/terms/identifier"doi:10.4049/jimmunol.1102899"xsd:string
http://purl.uniprot.org/citations/22387553http://purl.uniprot.org/core/author"Liu Z."xsd:string
http://purl.uniprot.org/citations/22387553http://purl.uniprot.org/core/author"Chang C.C."xsd:string
http://purl.uniprot.org/citations/22387553http://purl.uniprot.org/core/author"Zhang Q.Y."xsd:string
http://purl.uniprot.org/citations/22387553http://purl.uniprot.org/core/author"Suciu-Foca N."xsd:string
http://purl.uniprot.org/citations/22387553http://purl.uniprot.org/core/author"Vlad G."xsd:string
http://purl.uniprot.org/citations/22387553http://purl.uniprot.org/core/author"Clynes R.A."xsd:string
http://purl.uniprot.org/citations/22387553http://purl.uniprot.org/core/date"2012"xsd:gYear
http://purl.uniprot.org/citations/22387553http://purl.uniprot.org/core/name"J Immunol"xsd:string
http://purl.uniprot.org/citations/22387553http://purl.uniprot.org/core/pages"3042-3052"xsd:string
http://purl.uniprot.org/citations/22387553http://purl.uniprot.org/core/title"Downregulation of inflammatory microRNAs by Ig-like transcript 3 is essential for the differentiation of human CD8(+) T suppressor cells."xsd:string
http://purl.uniprot.org/citations/22387553http://purl.uniprot.org/core/volume"188"xsd:string
http://purl.uniprot.org/citations/22387553http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/22387553
http://purl.uniprot.org/citations/22387553http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/22387553
http://purl.uniprot.org/uniprot/Q9Y6W6#attribution-5C6666880621D8A0E4FC5EF9DBE34FB8http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/22387553
http://purl.uniprot.org/uniprot/P53539#attribution-8B64F1614CAAC3E3760427E43A52ED6Ehttp://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/22387553
http://purl.uniprot.org/uniprot/P01100#attribution-8B64F1614CAAC3E3760427E43A52ED6Ehttp://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/22387553
http://purl.uniprot.org/uniprot/Q8NHJ6#attribution-8B64F1614CAAC3E3760427E43A52ED6Ehttp://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/22387553
http://purl.uniprot.org/uniprot/O15524#attribution-5C6666880621D8A0E4FC5EF9DBE34FB8http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/22387553