pubmed-article:19563342 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:19563342 | lifeskim:mentions | umls-concept:C1332717 | lld:lifeskim |
pubmed-article:19563342 | lifeskim:mentions | umls-concept:C1706438 | lld:lifeskim |
pubmed-article:19563342 | lifeskim:mentions | umls-concept:C0225336 | lld:lifeskim |
pubmed-article:19563342 | lifeskim:mentions | umls-concept:C0085358 | lld:lifeskim |
pubmed-article:19563342 | lifeskim:mentions | umls-concept:C1704632 | lld:lifeskim |
pubmed-article:19563342 | lifeskim:mentions | umls-concept:C0871261 | lld:lifeskim |
pubmed-article:19563342 | lifeskim:mentions | umls-concept:C0205276 | lld:lifeskim |
pubmed-article:19563342 | lifeskim:mentions | umls-concept:C0009528 | lld:lifeskim |
pubmed-article:19563342 | lifeskim:mentions | umls-concept:C1413244 | lld:lifeskim |
pubmed-article:19563342 | lifeskim:mentions | umls-concept:C2698600 | lld:lifeskim |
pubmed-article:19563342 | lifeskim:mentions | umls-concept:C2911692 | lld:lifeskim |
pubmed-article:19563342 | lifeskim:mentions | umls-concept:C1706817 | lld:lifeskim |
pubmed-article:19563342 | lifeskim:mentions | umls-concept:C0332298 | lld:lifeskim |
pubmed-article:19563342 | lifeskim:mentions | umls-concept:C1515895 | lld:lifeskim |
pubmed-article:19563342 | pubmed:issue | 8 | lld:pubmed |
pubmed-article:19563342 | pubmed:dateCreated | 2009-8-7 | lld:pubmed |
pubmed-article:19563342 | pubmed:abstractText | CD8 T cells primed by transplantation recognize allogeneic class I MHC molecules expressed on graft vascular endothelium and contribute to allograft injury. We previously showed that immune cell-derived complement activation fragments are integral to T cell activation/expansion. Herein we tested the impact of local complement production/activation on T cell/endothelial cell (EC) interactions. We found that proinflammatory cytokines upregulated alternative pathway complement production by ECs, yielding C5a. We further found that ECs deficient in the cell surface C3/C5 convertase regulator decay accelerating factor (DAF, CD55) induced greater CD8 T-cell proliferation and more IFNgamma(+) and perforin(+) effector cells than wild-type (WT) ECs. Allogeneic C3(-/-) EC induced little or no CD8 responses. Abrogation of responses following C5a receptor (C5aR) blockade, or augmentation following addition of recombinant C5a demonstrated that the effects were mediated through T-cell-expressed-C5aR interactions. Analyses of in vivo CD8 cell responses to transplanted heart grafts deficient in EC DAF showed similar augmentation. The findings reveal that EC-derived complement triggers secondary CD8 T-cell differentiation and expansion and argue that targeting complement and/or C5aR could limit T-cell-mediated graft injury. | lld:pubmed |
pubmed-article:19563342 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19563342 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19563342 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19563342 | pubmed:language | eng | lld:pubmed |
pubmed-article:19563342 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19563342 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:19563342 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:19563342 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19563342 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19563342 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19563342 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:19563342 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19563342 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:19563342 | pubmed:month | Aug | lld:pubmed |
pubmed-article:19563342 | pubmed:issn | 1600-6143 | lld:pubmed |
pubmed-article:19563342 | pubmed:author | pubmed-author:YangMM | lld:pubmed |
pubmed-article:19563342 | pubmed:author | pubmed-author:MedofM EME | lld:pubmed |
pubmed-article:19563342 | pubmed:author | pubmed-author:HeegerP SPS | lld:pubmed |
pubmed-article:19563342 | pubmed:author | pubmed-author:RaedlerHH | lld:pubmed |
pubmed-article:19563342 | pubmed:author | pubmed-author:LalliP NPN | lld:pubmed |
pubmed-article:19563342 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:19563342 | pubmed:volume | 9 | lld:pubmed |
pubmed-article:19563342 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:19563342 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:19563342 | pubmed:pagination | 1784-95 | lld:pubmed |
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pubmed-article:19563342 | pubmed:year | 2009 | lld:pubmed |
pubmed-article:19563342 | pubmed:articleTitle | Primed CD8(+) T-cell responses to allogeneic endothelial cells are controlled by local complement activation. | lld:pubmed |
pubmed-article:19563342 | pubmed:affiliation | Department of Medicine, Recanati Transplant Institute, Mount Sinai School of Medicine, New York, NY, USA. | lld:pubmed |
pubmed-article:19563342 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:19563342 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
pubmed-article:19563342 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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