Source:http://linkedlifedata.com/resource/pubmed/id/16887977
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
4
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| pubmed:dateCreated |
2006-8-4
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| pubmed:abstractText |
The ability of dendritic cells (DC) to initiate immune responses or induce immune tolerance is strictly dependent on their maturation state. TNF-alpha plays a pivotal role in the differentiation and maturation of DC. Blockade of TNF-alpha action may arrest DC in an immature state, prolonging their window of tolerogenic opportunity. Immature DC (imDC) were transfected with recombinant adenovirus to express soluble TNF-alpha receptor type I (sTNFRI), a specific inhibitor of TNF-alpha. The capacity of sTNFRI gene-modified imDC (DC-sTNFRI) to induce immune tolerance was analyzed. sTNFRI expression renders imDC resistant to maturation induction and impairs their capacity to migrate or present Ag. This process leads to induction of allogeneic T cell hyporesponsiveness and the generation of IL-10-producing T regulatory-like cells. In vivo pretreatment of transplant recipients with DC-sTNFRI induces long-term survival of cardiac allografts in 50% of cases, and leads to a substantial increase in the generation of microchimerism and T regulatory cell numbers. Thus, blockade of TNF-alpha action by sTNFRI genetic modification can inhibit the maturation of DC and potentiate the in vivo capacity of imDC to induce donor-specific immune tolerance and prolong allograft survival.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
AIM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Aug
|
| pubmed:issn |
0022-1767
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| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
15
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| pubmed:volume |
177
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
2175-85
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| pubmed:dateRevised |
2008-11-21
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| pubmed:meshHeading |
pubmed-meshheading:16887977-Animals,
pubmed-meshheading:16887977-Antigen Presentation,
pubmed-meshheading:16887977-Cell Differentiation,
pubmed-meshheading:16887977-Cells, Cultured,
pubmed-meshheading:16887977-Dendritic Cells,
pubmed-meshheading:16887977-Heart Transplantation,
pubmed-meshheading:16887977-Immunity, Innate,
pubmed-meshheading:16887977-Lymphocyte Activation,
pubmed-meshheading:16887977-Male,
pubmed-meshheading:16887977-Mice,
pubmed-meshheading:16887977-Mice, Inbred BALB C,
pubmed-meshheading:16887977-Mice, Inbred C3H,
pubmed-meshheading:16887977-Mice, Inbred C57BL,
pubmed-meshheading:16887977-Receptors, Tumor Necrosis Factor, Type I,
pubmed-meshheading:16887977-Skin Transplantation,
pubmed-meshheading:16887977-Solubility,
pubmed-meshheading:16887977-T-Lymphocytes, Regulatory,
pubmed-meshheading:16887977-Transfection,
pubmed-meshheading:16887977-Transplantation Tolerance,
pubmed-meshheading:16887977-Tumor Necrosis Factor-alpha
|
| pubmed:year |
2006
|
| pubmed:articleTitle |
Induction of allospecific tolerance by immature dendritic cells genetically modified to express soluble TNF receptor.
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| pubmed:affiliation |
Institute of Immunology, Second Military Medical University, 800 Yiangyin Road, Shanghai 200433, People's Republic of China.
|
| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|