| pubmed-article:15591115 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15591115 | lifeskim:mentions | umls-concept:C0005953 | lld:lifeskim |
| pubmed-article:15591115 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
| pubmed-article:15591115 | lifeskim:mentions | umls-concept:C1257975 | lld:lifeskim |
| pubmed-article:15591115 | lifeskim:mentions | umls-concept:C1293097 | lld:lifeskim |
| pubmed-article:15591115 | lifeskim:mentions | umls-concept:C0221117 | lld:lifeskim |
| pubmed-article:15591115 | lifeskim:mentions | umls-concept:C0237477 | lld:lifeskim |
| pubmed-article:15591115 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:15591115 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:15591115 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:15591115 | pubmed:dateCreated | 2005-3-22 | lld:pubmed |
| pubmed-article:15591115 | pubmed:abstractText | It has been shown that mesenchymal stem cells (MSCs) induce T cells to become unresponsive. We characterized the phenotype of these T cells by dissecting the effect of MSCs on T-cell activation, proliferation, and effector function. For this purpose, an in vitro murine model was used in which T-cell responses were generated against the male HY minor histocompatibility antigen. In the presence of MSCs, the expression of early activation markers CD25 and CD69 was unaffected but interferon-gamma (IFN-gamma) production was reduced. The inhibitory effect of MSCs was directed mainly at the level of cell proliferation. Analysis of the cell cycle showed that T cells, stimulated in the presence of MSCs, were arrested at the G1 phase. At the molecular level, cyclin D2 expression was profoundly inhibited, whereas p27(kip1) was up-regulated. When MSCs were removed from the cultures and restimulated with the cognate peptide, T cells produced IFN-gamma but failed to proliferate. The addition of exogenous interleukin-2 (IL-2) did not restore proliferation. MSCs did not preferentially target any T-cell subset, and the inhibition was also extended to B cells. MSC-mediated inhibition induces an unresponsive T-cell profile that is fully consistent with that observed in division arrest anergy. | lld:pubmed |
| pubmed-article:15591115 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15591115 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15591115 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:15591115 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15591115 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:15591115 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15591115 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15591115 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:15591115 | pubmed:issn | 0006-4971 | lld:pubmed |
| pubmed-article:15591115 | pubmed:author | pubmed-author:LamEric W-FEW | lld:pubmed |
| pubmed-article:15591115 | pubmed:author | pubmed-author:GlennieSarahS | lld:pubmed |
| pubmed-article:15591115 | pubmed:author | pubmed-author:DazziFrancesc... | lld:pubmed |
| pubmed-article:15591115 | pubmed:author | pubmed-author:SoeiroInêsI | lld:pubmed |
| pubmed-article:15591115 | pubmed:author | pubmed-author:DysonPeter... | lld:pubmed |
| pubmed-article:15591115 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15591115 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:15591115 | pubmed:volume | 105 | lld:pubmed |
| pubmed-article:15591115 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15591115 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15591115 | pubmed:pagination | 2821-7 | lld:pubmed |
| pubmed-article:15591115 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:15591115 | pubmed:year | 2005 | lld:pubmed |
| pubmed-article:15591115 | pubmed:articleTitle | Bone marrow mesenchymal stem cells induce division arrest anergy of activated T cells. | lld:pubmed |
| pubmed-article:15591115 | pubmed:affiliation | Department of Immunology and Transplantation Biology, Faculty of Medicine, Imperial College London, United Kingdom. | lld:pubmed |
| pubmed-article:15591115 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15591115 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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