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http://purl.uniprot.org/citations/23682316http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/23682316http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/23682316http://www.w3.org/2000/01/rdf-schema#comment"Splenic dendritic cells (DCs) present blood-borne antigens to lymphocytes to promote T cell and antibody responses. The cues involved in positioning DCs in areas of antigen exposure in the spleen are undefined. Here we show that CD4(+) DCs highly express EBI2 and migrate to its oxysterol ligand, 7α,25-OHC. In mice lacking EBI2 or the enzymes needed for generating normal distributions of 7α,25-OHC, CD4(+) DCs are reduced in frequency and the remaining cells fail to situate in marginal zone bridging channels. The CD4(+) DC deficiency can be rescued by LTβR agonism. EBI2-mediated positioning in bridging channels promotes DC encounter with blood-borne particulate antigen. Upon exposure to antigen, CD4(+) DCs move rapidly to the T-B zone interface and promote induction of helper T cell and antibody responses. These findings establish an essential role for EBI2 in CD4(+) DC positioning and homeostasis and in facilitating capture and presentation of blood-borne particulate antigens. DOI:http://dx.doi.org/10.7554/eLife.00757.001."xsd:string
http://purl.uniprot.org/citations/23682316http://purl.org/dc/terms/identifier"doi:10.7554/elife.00757"xsd:string
http://purl.uniprot.org/citations/23682316http://purl.org/dc/terms/identifier"doi:10.7554/elife.00757"xsd:string
http://purl.uniprot.org/citations/23682316http://purl.uniprot.org/core/author"Cyster J.G."xsd:string
http://purl.uniprot.org/citations/23682316http://purl.uniprot.org/core/author"Cyster J.G."xsd:string
http://purl.uniprot.org/citations/23682316http://purl.uniprot.org/core/author"Yi T."xsd:string
http://purl.uniprot.org/citations/23682316http://purl.uniprot.org/core/author"Yi T."xsd:string
http://purl.uniprot.org/citations/23682316http://purl.uniprot.org/core/date"2013"xsd:gYear
http://purl.uniprot.org/citations/23682316http://purl.uniprot.org/core/date"2013"xsd:gYear
http://purl.uniprot.org/citations/23682316http://purl.uniprot.org/core/name"Elife"xsd:string
http://purl.uniprot.org/citations/23682316http://purl.uniprot.org/core/name"Elife"xsd:string
http://purl.uniprot.org/citations/23682316http://purl.uniprot.org/core/pages"E00757"xsd:string
http://purl.uniprot.org/citations/23682316http://purl.uniprot.org/core/pages"E00757"xsd:string
http://purl.uniprot.org/citations/23682316http://purl.uniprot.org/core/title"EBI2-mediated bridging channel positioning supports splenic dendritic cell homeostasis and particulate antigen capture."xsd:string
http://purl.uniprot.org/citations/23682316http://purl.uniprot.org/core/title"EBI2-mediated bridging channel positioning supports splenic dendritic cell homeostasis and particulate antigen capture."xsd:string
http://purl.uniprot.org/citations/23682316http://purl.uniprot.org/core/volume"2"xsd:string
http://purl.uniprot.org/citations/23682316http://purl.uniprot.org/core/volume"2"xsd:string
http://purl.uniprot.org/citations/23682316http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/23682316
http://purl.uniprot.org/citations/23682316http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/23682316
http://purl.uniprot.org/citations/23682316http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/23682316
http://purl.uniprot.org/citations/23682316http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/23682316
http://purl.uniprot.org/uniprot/Q3U6B2http://purl.uniprot.org/core/citationhttp://purl.uniprot.org/citations/23682316
http://purl.uniprot.org/uniprot/Q3U6B2#attribution-32F945957FB3FC4F27BAE88C602EB506http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/23682316