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http://purl.uniprot.org/citations/27444337http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/27444337http://www.w3.org/2000/01/rdf-schema#comment"B cells have an important pathogenic role in the development of type 1 diabetes in the non-obese diabetic (NOD) mouse. We have previously reported that NOD mice display an increased percentage of TACIhigh -expressing B cells compared with C57BL/6 mice and this trait is linked to chromosomes 1 and 8. In this paper the genetic association of the transmembrane activator, calcium modulator and cyclophilin ligand interactor (TACI) trait was confirmed using double congenic NOD.B6C1/Idd22 mice. TACI ligation by a proliferation-inducing ligand (APRIL) has been shown to influence plasma cell differentiation, immunoglobulin production and isotype switch. Hence, the functional consequence of the up-regulation of TACI on NOD B cells was analysed both in vitro and in vivo. NOD B cells stimulated with APRIL showed an enhanced plasma cell differentiation and class switch to IgG and IgA compared with B cells from C57BL/6 mice. Moreover, flow cytometry analyses revealed that germinal centre B cells in NOD failed to down-regulate TACI. Availability of the TACI ligand B-cell activating factor (BAFF) has been shown to be a limiting factor in the germinal centre reaction. In line with this, upon immunization with 4-hydroxy-3-nitrophenylacetyl hapten-conjugated hen egg lysozyme, NOD mice produced higher titres of low-affinity antibodies compared with C57BL/6 mice. This observation was supported by the detection of increased levels of BAFF in NOD germinal centres after immunization compared with C57BL/6 by immunofluorescence. Our results support the hypothesis that increased TACI expression on NOD B cells contributes to the pathogenesis of type 1 diabetes in the NOD mouse."xsd:string
http://purl.uniprot.org/citations/27444337http://purl.org/dc/terms/identifier"doi:10.1111/imm.12651"xsd:string
http://purl.uniprot.org/citations/27444337http://purl.uniprot.org/core/author"Sundstrom M."xsd:string
http://purl.uniprot.org/citations/27444337http://purl.uniprot.org/core/author"Lejon K."xsd:string
http://purl.uniprot.org/citations/27444337http://purl.uniprot.org/core/author"Banday V.S."xsd:string
http://purl.uniprot.org/citations/27444337http://purl.uniprot.org/core/author"Thyagarajan R."xsd:string
http://purl.uniprot.org/citations/27444337http://purl.uniprot.org/core/date"2016"xsd:gYear
http://purl.uniprot.org/citations/27444337http://purl.uniprot.org/core/name"Immunology"xsd:string
http://purl.uniprot.org/citations/27444337http://purl.uniprot.org/core/pages"297-305"xsd:string
http://purl.uniprot.org/citations/27444337http://purl.uniprot.org/core/title"Increased expression of TACI on NOD B cells results in germinal centre reaction anomalies, enhanced plasma cell differentiation and immunoglobulin production."xsd:string
http://purl.uniprot.org/citations/27444337http://purl.uniprot.org/core/volume"149"xsd:string
http://purl.uniprot.org/citations/27444337http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/27444337
http://purl.uniprot.org/citations/27444337http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/27444337
http://purl.uniprot.org/uniprot/#_A5D8Y6-mappedCitation-27444337http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/27444337
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http://purl.uniprot.org/uniprot/#_Q9ET35-mappedCitation-27444337http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/27444337
http://purl.uniprot.org/uniprot/A5D8Y6http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/27444337
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