| pubmed-article:21248258 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:21248258 | lifeskim:mentions | umls-concept:C0038013 | lld:lifeskim |
| pubmed-article:21248258 | lifeskim:mentions | umls-concept:C2936411 | lld:lifeskim |
| pubmed-article:21248258 | lifeskim:mentions | umls-concept:C0019740 | lld:lifeskim |
| pubmed-article:21248258 | lifeskim:mentions | umls-concept:C0205217 | lld:lifeskim |
| pubmed-article:21248258 | lifeskim:mentions | umls-concept:C1416653 | lld:lifeskim |
| pubmed-article:21248258 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:21248258 | pubmed:dateCreated | 2011-2-3 | lld:pubmed |
| pubmed-article:21248258 | pubmed:abstractText | CD4 Th cells producing the proinflammatory cytokine IL-17 (Th17) have been implicated in a number of inflammatory arthritides including the spondyloarthritides. Th17 development is promoted by IL-23. Ankylosing spondylitis, the most common spondyloarthritis (SpA), is genetically associated with both HLA-B27 (B27) and IL-23R polymorphisms; however, the link remains unexplained. We have previously shown that B27 can form H chain dimers (termed B27(2)), which, unlike classical HLA-B27, bind the killer-cell Ig-like receptor KIR3DL2. In this article, we show that B27(2)-expressing APCs stimulate the survival, proliferation, and IL-17 production of KIR3DL2(+) CD4 T cells. KIR3DL2(+) CD4 T cells are expanded and enriched for IL-17 production in the blood and synovial fluid of patients with SpA. Despite KIR3DL2(+) cells comprising a mean of just 15% of CD4 T in the peripheral blood of SpA patients, this subset accounted for 70% of the observed increase in Th17 numbers in SpA patients compared with control subjects. TCR-stimulated peripheral blood KIR3DL2(+) CD4 T cell lines from SpA patients secreted 4-fold more IL-17 than KIR3DL2(+) lines from controls or KIR3DL2(-) CD4 T cells. Strikingly, KIR3DL2(+) CD4 T cells account for the majority of peripheral blood CD4 T cell IL-23R expression and produce more IL-17 in the presence of IL-23. Our findings link HLA-B27 with IL-17 production and suggest new therapeutic strategies in ankylosing spondylitis/SpA. | lld:pubmed |
| pubmed-article:21248258 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21248258 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21248258 | pubmed:language | eng | lld:pubmed |
| pubmed-article:21248258 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21248258 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:21248258 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21248258 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:21248258 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21248258 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21248258 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21248258 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:21248258 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:21248258 | pubmed:issn | 1550-6606 | lld:pubmed |
| pubmed-article:21248258 | pubmed:author | pubmed-author:McMichaelAndr... | lld:pubmed |
| pubmed-article:21248258 | pubmed:author | pubmed-author:BownessPaulP | lld:pubmed |
| pubmed-article:21248258 | pubmed:author | pubmed-author:KollnbergerSi... | lld:pubmed |
| pubmed-article:21248258 | pubmed:author | pubmed-author:ShawJacquelin... | lld:pubmed |
| pubmed-article:21248258 | pubmed:author | pubmed-author:Wong-BaezaIsa... | lld:pubmed |
| pubmed-article:21248258 | pubmed:author | pubmed-author:CummingsFrase... | lld:pubmed |
| pubmed-article:21248258 | pubmed:author | pubmed-author:RidleyAnnaA | lld:pubmed |
| pubmed-article:21248258 | pubmed:author | pubmed-author:ChanAntoni... | lld:pubmed |
| pubmed-article:21248258 | pubmed:author | pubmed-author:FlemingMylesM | lld:pubmed |
| pubmed-article:21248258 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:21248258 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:21248258 | pubmed:volume | 186 | lld:pubmed |
| pubmed-article:21248258 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:21248258 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:21248258 | pubmed:pagination | 2672-80 | lld:pubmed |
| pubmed-article:21248258 | pubmed:dateRevised | 2011-11-11 | lld:pubmed |
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| pubmed-article:21248258 | pubmed:meshHeading | pubmed-meshheading:21248258... | lld:pubmed |
| pubmed-article:21248258 | pubmed:year | 2011 | lld:pubmed |
| pubmed-article:21248258 | pubmed:articleTitle | Th17 cells expressing KIR3DL2+ and responsive to HLA-B27 homodimers are increased in ankylosing spondylitis. | lld:pubmed |
| pubmed-article:21248258 | pubmed:affiliation | Medical Research Council Human Immunology Unit, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, Headington, Oxford OX3 9DS, United Kingdom. | lld:pubmed |
| pubmed-article:21248258 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:21248258 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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