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http://purl.uniprot.org/citations/22487925http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/22487925http://www.w3.org/2000/01/rdf-schema#comment"

Aims/hypothesis

The aim of this study was to understand the role of CXC chemokine receptor 3 (CXCR3), a T-helper 1(Th1) type chemokine receptor, in the pathogenesis of type 1 diabetes.

Methods

We observed the incidence of diabetes in Cxcr3 homozygous knockout mice. We compared the expression pattern of various cytokines and chemokines and the frequency of FOXP3(+) cells in the pancreas and pancreatic lymph nodes from Cxcr3 ( -/-) NOD mice and wild-type NOD mice. In addition, we observed the migration ability of CXCR3(+)CD4(+) cells to pancreatic islets upon adoptive transfer. Finally, we examined whether Cxcr3 (+) regulatory T cells (Tregs) actually suppressed the onset of diabetes in vivo.

Results

Cxcr3 ( -/-) NOD mice developed spontaneous diabetes earlier than did wild-type NOD mice. In Cxcr3 ( -/-) NOD mice, Tregs were more frequent in pancreatic lymph nodes and less frequent in pancreatic islets than in wild-type NOD mice. While transferred CXCR3(-)CD4(+) cells from wild-type NOD mice did not infiltrate pancreatic islets of NOD-severe combined immunodeficiency (SCID) mice, CXCR3(+)CD4(+) cells from the same mice migrated into the recipient islets and contained Forkhead box P3 (FOXP3) upon adoptive transfer. Moreover, CD4(+)CD25(+) cells from wild-type NOD mice suppressed and delayed the onset of diabetes compared with those from Cxcr3 ( -/-) NOD mice in a cyclophosphamide-induced diabetes model system.

Conclusions/interpretation

The mechanism of accelerated diabetes onset in Cxcr3 ( -/-) NOD mice was considered to be due to the lack of hybrid Tregs (CXCR3(+)FOXP3(+)CD4(+) cells), which could effectively migrate into and regulate Th1 inflammation in local lesions under Cxcr3 knockout conditions."xsd:string
http://purl.uniprot.org/citations/22487925http://purl.org/dc/terms/identifier"doi:10.1007/s00125-012-2547-8"xsd:string
http://purl.uniprot.org/citations/22487925http://purl.uniprot.org/core/author"Itoh H."xsd:string
http://purl.uniprot.org/citations/22487925http://purl.uniprot.org/core/author"Yamada Y."xsd:string
http://purl.uniprot.org/citations/22487925http://purl.uniprot.org/core/author"Yamada S."xsd:string
http://purl.uniprot.org/citations/22487925http://purl.uniprot.org/core/author"Shimada A."xsd:string
http://purl.uniprot.org/citations/22487925http://purl.uniprot.org/core/author"Okubo Y."xsd:string
http://purl.uniprot.org/citations/22487925http://purl.uniprot.org/core/author"Matsushima K."xsd:string
http://purl.uniprot.org/citations/22487925http://purl.uniprot.org/core/author"Oikawa Y."xsd:string
http://purl.uniprot.org/citations/22487925http://purl.uniprot.org/core/author"Narumi S."xsd:string
http://purl.uniprot.org/citations/22487925http://purl.uniprot.org/core/date"2012"xsd:gYear
http://purl.uniprot.org/citations/22487925http://purl.uniprot.org/core/name"Diabetologia"xsd:string
http://purl.uniprot.org/citations/22487925http://purl.uniprot.org/core/pages"2238-2245"xsd:string
http://purl.uniprot.org/citations/22487925http://purl.uniprot.org/core/title"Acceleration of diabetes development in CXC chemokine receptor 3 (CXCR3)-deficient NOD mice."xsd:string
http://purl.uniprot.org/citations/22487925http://purl.uniprot.org/core/volume"55"xsd:string
http://purl.uniprot.org/citations/22487925http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/22487925
http://purl.uniprot.org/citations/22487925http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/22487925
http://purl.uniprot.org/uniprot/#_O88410-mappedCitation-22487925http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22487925
http://purl.uniprot.org/uniprot/O88410http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/22487925