Source:http://linkedlifedata.com/resource/pubmed/id/15591115
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
7
|
| pubmed:dateCreated |
2005-3-22
|
| 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.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
AIM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Apr
|
| pubmed:issn |
0006-4971
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| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
1
|
| pubmed:volume |
105
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
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| pubmed:pagination |
2821-7
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| pubmed:dateRevised |
2009-11-19
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| pubmed:meshHeading |
pubmed-meshheading:15591115-Animals,
pubmed-meshheading:15591115-B-Lymphocytes,
pubmed-meshheading:15591115-Bone Marrow Cells,
pubmed-meshheading:15591115-CD4-Positive T-Lymphocytes,
pubmed-meshheading:15591115-CD8-Positive T-Lymphocytes,
pubmed-meshheading:15591115-Cell Communication,
pubmed-meshheading:15591115-Cell Division,
pubmed-meshheading:15591115-Cyclin D2,
pubmed-meshheading:15591115-Cyclins,
pubmed-meshheading:15591115-DNA,
pubmed-meshheading:15591115-Down-Regulation,
pubmed-meshheading:15591115-Flow Cytometry,
pubmed-meshheading:15591115-G0 Phase,
pubmed-meshheading:15591115-G1 Phase,
pubmed-meshheading:15591115-Lymphocyte Activation,
pubmed-meshheading:15591115-Mesoderm,
pubmed-meshheading:15591115-Mice,
pubmed-meshheading:15591115-Mice, Inbred BALB C,
pubmed-meshheading:15591115-Mice, Inbred C57BL,
pubmed-meshheading:15591115-Mice, Inbred CBA,
pubmed-meshheading:15591115-Mice, Transgenic
|
| pubmed:year |
2005
|
| pubmed:articleTitle |
Bone marrow mesenchymal stem cells induce division arrest anergy of activated T cells.
|
| pubmed:affiliation |
Department of Immunology and Transplantation Biology, Faculty of Medicine, Imperial College London, United Kingdom.
|
| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|