Source:http://linkedlifedata.com/resource/pubmed/id/20939892
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
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pubmed:dateCreated |
2010-11-25
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pubmed:abstractText |
Chemokines and their receptors are potential therapeutic targets in rheumatoid arthritis (RA). Among these, several studies suggested the involvement of CXC chemokine 4 (CXCR4) and its ligand CXC ligand 12 (SDF-1) in RA pathogenesis. However, the role of these molecules in T-cell function is not known completely because of embryonic lethality of Cxcr4- and Cxcl12-deficient mice. In this report, we generated T cell-specific Cxcr4-deficient mice and showed that the CXCR4 in T cells is important for the development of collagen-induced arthritis (CIA).
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:issn |
1478-6362
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
12
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
R188
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pubmed:meshHeading |
pubmed-meshheading:20939892-Animals,
pubmed-meshheading:20939892-Arthritis, Experimental,
pubmed-meshheading:20939892-Arthritis, Rheumatoid,
pubmed-meshheading:20939892-Cell Separation,
pubmed-meshheading:20939892-Chemokine CXCL12,
pubmed-meshheading:20939892-Chemotaxis, Leukocyte,
pubmed-meshheading:20939892-Flow Cytometry,
pubmed-meshheading:20939892-Immunohistochemistry,
pubmed-meshheading:20939892-Mice,
pubmed-meshheading:20939892-Mice, Transgenic,
pubmed-meshheading:20939892-Receptors, CXCR4,
pubmed-meshheading:20939892-T-Lymphocytes
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pubmed:year |
2010
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pubmed:articleTitle |
CXC chemokine receptor 4 expressed in T cells plays an important role in the development of collagen-induced arthritis.
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pubmed:affiliation |
Laboratory of Molecular Pathogenesis, Center for Experimental Medicine and Systems Biology, Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan. shchung@ims.u-tokyo.ac.jp
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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