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http://purl.uniprot.org/citations/18195070http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/18195070http://www.w3.org/2000/01/rdf-schema#comment"Self-antigens expressed by apoptotic cells (ACs) may become targets for autoimmunity. Tolerance to these antigens is partly established by an ill-defined capacity of ACs to inhibit antigen-presenting cells such as dendritic cells (DCs). We present evidence that the receptor tyrosine kinase Mer (MerTK) has a key role in mediating AC-induced inhibition of DC activation/maturation. Pretreatment of DCs prepared from nonobese diabetic (NOD) mice with AC blocked secretion of proinflammatory cytokines, up-regulation of costimulatory molecule expression, and T cell activation. The effect of ACs on DCs was dependent on Gas6, which is a MerTK ligand. NOD DCs lacking MerTK expression (NOD.MerTK(KD/KD)) were resistant to AC-induced inhibition. Notably, autoimmune diabetes was exacerbated in NOD.MerTK(KD/KD) versus NOD mice expressing the transgenic BDC T cell receptor. In addition, beta cell-specific CD4(+) T cells adoptively transferred into NOD.MerTK(KD/KD) mice in which beta cell apoptosis was induced with streptozotocin exhibited increased expansion and differentiation into type 1 T cell effectors. In both models, the lack of MerTK expression was associated with an increased frequency of activated pancreatic CD11c(+)CD8alpha(+) DCs, which exhibited an enhanced T cell stimulatory capacity. These findings demonstrate that MerTK plays a critical role in regulating self-tolerance mediated between ACs, DCs, and T cells."xsd:string
http://purl.uniprot.org/citations/18195070http://purl.org/dc/terms/identifier"doi:10.1084/jem.20062293"xsd:string
http://purl.uniprot.org/citations/18195070http://purl.uniprot.org/core/author"Huang Y."xsd:string
http://purl.uniprot.org/citations/18195070http://purl.uniprot.org/core/author"Wang Y."xsd:string
http://purl.uniprot.org/citations/18195070http://purl.uniprot.org/core/author"Wang B."xsd:string
http://purl.uniprot.org/citations/18195070http://purl.uniprot.org/core/author"Sen P."xsd:string
http://purl.uniprot.org/citations/18195070http://purl.uniprot.org/core/author"Earp H.S."xsd:string
http://purl.uniprot.org/citations/18195070http://purl.uniprot.org/core/author"Yi Z."xsd:string
http://purl.uniprot.org/citations/18195070http://purl.uniprot.org/core/author"Mathews C.E."xsd:string
http://purl.uniprot.org/citations/18195070http://purl.uniprot.org/core/author"Tisch R."xsd:string
http://purl.uniprot.org/citations/18195070http://purl.uniprot.org/core/author"Wallet M.A."xsd:string
http://purl.uniprot.org/citations/18195070http://purl.uniprot.org/core/author"Matsushima G."xsd:string
http://purl.uniprot.org/citations/18195070http://purl.uniprot.org/core/author"Flores R.R."xsd:string
http://purl.uniprot.org/citations/18195070http://purl.uniprot.org/core/date"2008"xsd:gYear
http://purl.uniprot.org/citations/18195070http://purl.uniprot.org/core/name"J Exp Med"xsd:string
http://purl.uniprot.org/citations/18195070http://purl.uniprot.org/core/pages"219-232"xsd:string
http://purl.uniprot.org/citations/18195070http://purl.uniprot.org/core/title"MerTK is required for apoptotic cell-induced T cell tolerance."xsd:string
http://purl.uniprot.org/citations/18195070http://purl.uniprot.org/core/volume"205"xsd:string
http://purl.uniprot.org/citations/18195070http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/18195070
http://purl.uniprot.org/citations/18195070http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/18195070
http://purl.uniprot.org/uniprot/#_Q8CE52-mappedCitation-18195070http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/18195070
http://purl.uniprot.org/uniprot/#_Q60805-mappedCitation-18195070http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/18195070
http://purl.uniprot.org/uniprot/#_Q8K3Z7-mappedCitation-18195070http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/18195070
http://purl.uniprot.org/uniprot/#_Q8C584-mappedCitation-18195070http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/18195070