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http://purl.uniprot.org/citations/19768696http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/19768696http://www.w3.org/2000/01/rdf-schema#comment"Although CD8+ Treg-mediated suppression has been described, CD8+ Treg remain poorly characterized. Here we identify a novel subset of CD8+ Treg that express latency-associated peptide (LAP) on their cell surface (CD8+LAP+ cells) and exhibit regulatory activity in vitro and in vivo. Only a small fraction of CD8+LAP+ cells express Foxp3 or CD25, although the expression levels of Foxp3 for these cells are higher than their LAP-counterparts. In addition to TGF-beta, CD8+LAP+ cells produce IFN-gamma, and these cells suppress EAE that is dependent on both TGF-beta and IFN-gamma. In an adoptive co-transfer model, CD8+LAP+ cells suppress myelin oligodendrocyte glycoprotein (MOG)-specific immune responses by inducing or expanding Foxp3+ cells and by inhibiting proliferation and IFN-gamma production in vivo. Furthermore, in vivo neutralization of IFN-gamma and studies with IFN-gamma-deficient mice demonstrate an important role for IFN-gamma production in the function of CD8+LAP+ cells. Our findings identify the underlying mechanisms that account for the immunoregulatory activity of CD8+ T cells and suggest that induction or amplification of CD8+LAP+ cells may be a therapeutic strategy to help control autoimmune processes."xsd:string
http://purl.uniprot.org/citations/19768696http://purl.org/dc/terms/identifier"doi:10.1002/eji.200939441"xsd:string
http://purl.uniprot.org/citations/19768696http://purl.uniprot.org/core/author"Yan B.S."xsd:string
http://purl.uniprot.org/citations/19768696http://purl.uniprot.org/core/author"Chen M.L."xsd:string
http://purl.uniprot.org/citations/19768696http://purl.uniprot.org/core/author"Weiner H.L."xsd:string
http://purl.uniprot.org/citations/19768696http://purl.uniprot.org/core/author"Kozoriz D."xsd:string
http://purl.uniprot.org/citations/19768696http://purl.uniprot.org/core/date"2009"xsd:gYear
http://purl.uniprot.org/citations/19768696http://purl.uniprot.org/core/name"Eur J Immunol"xsd:string
http://purl.uniprot.org/citations/19768696http://purl.uniprot.org/core/pages"3423-3435"xsd:string
http://purl.uniprot.org/citations/19768696http://purl.uniprot.org/core/title"Novel CD8+ Treg suppress EAE by TGF-beta- and IFN-gamma-dependent mechanisms."xsd:string
http://purl.uniprot.org/citations/19768696http://purl.uniprot.org/core/volume"39"xsd:string
http://purl.uniprot.org/citations/19768696http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/19768696
http://purl.uniprot.org/citations/19768696http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/19768696
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http://purl.uniprot.org/uniprot/#_A0A078BCJ0-mappedCitation-19768696http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/19768696
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http://purl.uniprot.org/uniprot/#_P15261-mappedCitation-19768696http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/19768696
http://purl.uniprot.org/uniprot/#_A0A7R8C347-mappedCitation-19768696http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/19768696
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http://purl.uniprot.org/uniprot/#_A0A510GAF6-mappedCitation-19768696http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/19768696
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