Source:http://linkedlifedata.com/resource/pubmed/id/12415259
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rdf:type | |
lifeskim:mentions | |
pubmed:dateCreated |
2002-11-28
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pubmed:abstractText |
T cell-mediated loss of insulin-secreting beta cells in the islets of Langerhans is the hallmark of type 1 diabetes. The molecular basis for the directed migration of autoreactive T cells leading to insulitis is presently unknown. Here we demonstrate that in response to inflammation, beta cells secrete the chemokines CXC ligand 10 and CXC ligand 9, which specifically attract T-effector cells via the CXC chemokine receptor 3. In mice deficient for this receptor, the onset of type 1 diabetes is substantially delayed. Thus, in the absence of known etiological agents, CXC receptor 3 represents a novel target for therapeutic interference early in type 1 diabetes.
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pubmed:language |
eng
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CXCL10,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokines, CXC,
http://linkedlifedata.com/resource/pubmed/chemical/Cxcr3 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, CXCR3,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Chemokine
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pubmed:status |
MEDLINE
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pubmed:author | |
pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1414-20
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pubmed:dateRevised |
2007-11-15
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pubmed:articleTitle |
Beta cells are responsible for CXCR3-mediated T-cell infiltration in insulitis.
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pubmed:affiliation |
Pediatric Immunology, Department of Research and the University Children's Hospital, Basel, Switzerland.
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