{"@context":{"@vocab":"https://cir.nii.ac.jp/schema/1.0/","rdfs":"http://www.w3.org/2000/01/rdf-schema#","dc":"http://purl.org/dc/elements/1.1/","dcterms":"http://purl.org/dc/terms/","foaf":"http://xmlns.com/foaf/0.1/","prism":"http://prismstandard.org/namespaces/basic/2.0/","cinii":"http://ci.nii.ac.jp/ns/1.0/","datacite":"https://schema.datacite.org/meta/kernel-4/","ndl":"http://ndl.go.jp/dcndl/terms/","jpcoar":"https://github.com/JPCOAR/schema/blob/master/2.0/"},"@id":"https://cir.nii.ac.jp/crid/1363670318449508736.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.4049/jimmunol.0713370"}},{"identifier":{"@type":"URI","@value":"https://academic.oup.com/jimmunol/article-pdf/182/6/3343/62723266/8734.pdf"}}],"dc:title":[{"@value":"Cutting Edge: The PTPN22 Allelic Variant Associated with Autoimmunity Impairs B Cell Signaling"}],"description":[{"type":"abstract","notation":[{"@value":"<jats:title>Abstract</jats:title>\n                  <jats:p>PTPN22 is a gene encoding the protein tyrosine phosphatase Lyp. A missense mutation changing residue 1858 from cytosine to thymidine (1858C/T) is associated with multiple autoimmune disorders. Studies have demonstrated that Lyp has an inhibitory effect on TCR signaling; however, the presence of autoantibodies in all of the diseases associated with the 1858T variant and recent evidence that Ca2+ flux is altered in B cells of 1858T carriers indicate a role for Lyp in B cell signaling. In this study we show that B cell signal transduction is impaired in individuals who express the variant. This defect in signaling is characterized by a deficit in proliferation, a decrease in phosphorylation of key signaling proteins, and is reversed by inhibition of Lyp. These findings suggest that the PTPN22 1858T variant alters BCR signaling and implicate B cells in the mechanism by which the PTPN22 1858T variant contributes to autoimmunity.</jats:p>"}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1380870229271071488","@type":"Researcher","foaf:name":[{"@value":"Adrian F Arechiga"}],"jpcoar:affiliationName":[{"@value":"Translational Research Program, Benaroya Research Institute at Virginia Mason , Seattle, WA 98101"}]},{"@id":"https://cir.nii.ac.jp/crid/1383670318449508736","@type":"Researcher","foaf:name":[{"@value":"Tania Habib"}],"jpcoar:affiliationName":[{"@value":"Translational Research Program, Benaroya Research Institute at Virginia Mason , Seattle, WA 98101"}]},{"@id":"https://cir.nii.ac.jp/crid/1383670318449508738","@type":"Researcher","foaf:name":[{"@value":"Yantao He"}],"jpcoar:affiliationName":[{"@value":"Department of Biochemistry and Molecular Biology, Indiana University School of Medicine , Indianapolis IN 46202"}]},{"@id":"https://cir.nii.ac.jp/crid/1383670318449508737","@type":"Researcher","foaf:name":[{"@value":"Xian Zhang"}],"jpcoar:affiliationName":[{"@value":"Department of Biochemistry and Molecular Biology, Indiana University School of Medicine , Indianapolis IN 46202"}]},{"@id":"https://cir.nii.ac.jp/crid/1383670318449508740","@type":"Researcher","foaf:name":[{"@value":"Zhong-Yin Zhang"}],"jpcoar:affiliationName":[{"@value":"Department of Biochemistry and Molecular Biology, Indiana University School of Medicine , Indianapolis IN 46202"}]},{"@id":"https://cir.nii.ac.jp/crid/1383670318449508739","@type":"Researcher","foaf:name":[{"@value":"Andrew Funk"}],"jpcoar:affiliationName":[{"@value":"Translational Research Program, Benaroya Research Institute at Virginia Mason , Seattle, WA 98101"}]},{"@id":"https://cir.nii.ac.jp/crid/1380870229271071489","@type":"Researcher","foaf:name":[{"@value":"Jane H Buckner"}],"jpcoar:affiliationName":[{"@value":"Translational Research Program, Benaroya Research Institute at Virginia Mason , Seattle, WA 98101"}]}],"publication":{"publicationIdentifier":[{"@type":"EISSN","@value":"15506606"},{"@type":"PISSN","@value":"00221767"}],"prism:publicationName":[{"@value":"The Journal of Immunology"}],"dc:publisher":[{"@value":"Oxford University Press (OUP)"}],"prism:publicationDate":"2009-03","prism:volume":"182","prism:number":"6","prism:startingPage":"3343","prism:endingPage":"3347"},"reviewed":"false","dc:rights":["https://academic.oup.com/pages/standard-publication-reuse-rights"],"url":[{"@id":"https://academic.oup.com/jimmunol/article-pdf/182/6/3343/62723266/8734.pdf"}],"createdAt":"2009-03-05","modifiedAt":"2026-01-28","relatedProduct":[{"@id":"https://cir.nii.ac.jp/crid/1360567181954502400","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Genetic basis of rheumatoid arthritis: A current review"}]},{"@id":"https://cir.nii.ac.jp/crid/1360846642500993920","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Genetics of autoimmune diseases: perspectives from genome-wide association studies"}]},{"@id":"https://cir.nii.ac.jp/crid/1390001204648700672","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@language":"en","@value":"Genetic background of tolerance breakdown in rheumatoid arthritis"},{"@language":"ja","@value":"関節リウマチにおける免疫寛容の破綻とその遺伝的背景"}]}],"dataSourceIdentifier":[{"@type":"CROSSREF","@value":"10.4049/jimmunol.0713370"},{"@type":"CROSSREF","@value":"10.1093/intimm/dxw002_references_DOI_B9zI5Clgha3D0W8lcakMqPk53lA"},{"@type":"CROSSREF","@value":"10.2177/jsci.33.48_references_DOI_B9zI5Clgha3D0W8lcakMqPk53lA"},{"@type":"CROSSREF","@value":"10.1016/j.bbrc.2014.07.085_references_DOI_B9zI5Clgha3D0W8lcakMqPk53lA"}]}