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http://purl.uniprot.org/citations/18390708http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/18390708http://www.w3.org/2000/01/rdf-schema#comment"The maintenance of T cell tolerance in the periphery proceeds through several mechanisms, including anergy, immuno-regulation, and deletion via apoptosis. We examined the mechanism underlying the induction of CD8 T cell peripheral tolerance to a self-Ag expressed on pancreatic islet beta-cells. Following adoptive transfer, Ag-specific clone 4 T cells underwent deletion independently of extrinsic death receptors, including Fas, TNFR1, or TNFR2. Additional experiments revealed that the induction of clone 4 T cell apoptosis during peripheral tolerance occurred via an intrinsic death pathway that could be inhibited by overexpression of Bcl-2 or targeted deletion of the proapoptotic molecule, Bim, thereby resulting in accumulation of activated clone 4 T cells. Over-expression of Bcl-2 in clone 4 T cells promoted the development of effector function and insulitis whereas Bim-/-clone 4 cells were not autoaggressive. Examination of the upstream molecular mechanisms contributing to clone 4 T cell apoptosis revealed that it proceeded in a p53, E2F1, and E2F2-independent manner. Taken together, these data reveal that initiation of clone 4 T cell apoptosis during the induction of peripheral tolerance to a cross-presented self-Ag occurs through a Bcl-2-sensitive and at least partially Bim-dependent mechanism."xsd:string
http://purl.uniprot.org/citations/18390708http://purl.org/dc/terms/identifier"doi:10.4049/jimmunol.180.8.5275"xsd:string
http://purl.uniprot.org/citations/18390708http://purl.uniprot.org/core/author"Sherman L.A."xsd:string
http://purl.uniprot.org/citations/18390708http://purl.uniprot.org/core/author"Wei C.H."xsd:string
http://purl.uniprot.org/citations/18390708http://purl.uniprot.org/core/author"Kreuwel H.T."xsd:string
http://purl.uniprot.org/citations/18390708http://purl.uniprot.org/core/author"Redmond W.L."xsd:string
http://purl.uniprot.org/citations/18390708http://purl.uniprot.org/core/date"2008"xsd:gYear
http://purl.uniprot.org/citations/18390708http://purl.uniprot.org/core/name"J Immunol"xsd:string
http://purl.uniprot.org/citations/18390708http://purl.uniprot.org/core/pages"5275-5282"xsd:string
http://purl.uniprot.org/citations/18390708http://purl.uniprot.org/core/title"The apoptotic pathway contributing to the deletion of naive CD8 T cells during the induction of peripheral tolerance to a cross-presented self-antigen."xsd:string
http://purl.uniprot.org/citations/18390708http://purl.uniprot.org/core/volume"180"xsd:string
http://purl.uniprot.org/citations/18390708http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/18390708
http://purl.uniprot.org/citations/18390708http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/18390708
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http://purl.uniprot.org/uniprot/#_A0A158SIS7-mappedCitation-18390708http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/18390708
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http://purl.uniprot.org/uniprot/#_A0A494BBE8-mappedCitation-18390708http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/18390708
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http://purl.uniprot.org/uniprot/#_A1Y9B2-mappedCitation-18390708http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/18390708
http://purl.uniprot.org/uniprot/#_D6RG55-mappedCitation-18390708http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/18390708
http://purl.uniprot.org/uniprot/#_I7HIK9-mappedCitation-18390708http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/18390708
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http://purl.uniprot.org/uniprot/#_Q62327-mappedCitation-18390708http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/18390708