pubmed-article:10933709 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:10933709 | lifeskim:mentions | umls-concept:C1564874 | lld:lifeskim |
pubmed-article:10933709 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
pubmed-article:10933709 | lifeskim:mentions | umls-concept:C0205252 | lld:lifeskim |
pubmed-article:10933709 | lifeskim:mentions | umls-concept:C0039195 | lld:lifeskim |
pubmed-article:10933709 | lifeskim:mentions | umls-concept:C0011306 | lld:lifeskim |
pubmed-article:10933709 | lifeskim:mentions | umls-concept:C1539081 | lld:lifeskim |
pubmed-article:10933709 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
pubmed-article:10933709 | lifeskim:mentions | umls-concept:C1515655 | lld:lifeskim |
pubmed-article:10933709 | lifeskim:mentions | umls-concept:C0442335 | lld:lifeskim |
pubmed-article:10933709 | pubmed:issue | 17 | lld:pubmed |
pubmed-article:10933709 | pubmed:dateCreated | 2000-9-14 | lld:pubmed |
pubmed-article:10933709 | pubmed:abstractText | Recombinant adeno-associated virus type 2 (rAAV) is being explored as a vector for gene therapy because of its broad host range, good safety profile, and persistent transgene expression in vivo. However, accumulating evidence indicates that administration of AAV vector may initiate a detectable cellular and humoral immune response to its transduced neo-antigen in vivo. To elucidate the cellular basis of the AAV-mediated immune response, C57BL/6 mouse bone marrow-derived immature and mature dendritic cells (DCs) were infected with AAV encoding beta-galactosidase (AAV-lacZ) and adoptively transferred into mice that had received an intramuscular injection of AAV-lacZ 10 days earlier. Unexpectedly, C57BL/6 mice but not CD40 ligand-deficient (CD40L(-/-)) mice adoptively transferred with AAV-lacZ-infected immature DCs developed a beta-galactosidase-specific cytotoxic T-lymphocyte (CTL) response that markedly diminished AAV-lacZ-transduced gene expression in muscle fibers. In contrast, adoptive transfer of AAV-lacZ-infected mature DCs failed to elicit a similar CTL response in vivo. Our findings indicate, for the first time, that immature DCs may be able to elicit a CD40L-dependent T-cell immunity to markedly diminish AAV-lacZ transduced gene expression in vivo when a sufficient number of DCs capturing rAAV vector and/or its transduced gene products is recruited. | lld:pubmed |
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pubmed-article:10933709 | pubmed:language | eng | lld:pubmed |
pubmed-article:10933709 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10933709 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:10933709 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:10933709 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10933709 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:10933709 | pubmed:month | Sep | lld:pubmed |
pubmed-article:10933709 | pubmed:issn | 0022-538X | lld:pubmed |
pubmed-article:10933709 | pubmed:author | pubmed-author:WilsonJJ | lld:pubmed |
pubmed-article:10933709 | pubmed:author | pubmed-author:ZhangYY | lld:pubmed |
pubmed-article:10933709 | pubmed:author | pubmed-author:ChirmuleNN | lld:pubmed |
pubmed-article:10933709 | pubmed:author | pubmed-author:CuiH MHM | lld:pubmed |
pubmed-article:10933709 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:10933709 | pubmed:volume | 74 | lld:pubmed |
pubmed-article:10933709 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:10933709 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:10933709 | pubmed:pagination | 8003-10 | lld:pubmed |
pubmed-article:10933709 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:10933709 | pubmed:year | 2000 | lld:pubmed |
pubmed-article:10933709 | pubmed:articleTitle | CD40 ligand-dependent activation of cytotoxic T lymphocytes by adeno-associated virus vectors in vivo: role of immature dendritic cells. | lld:pubmed |
pubmed-article:10933709 | pubmed:affiliation | Institute for Human Gene Therapy and Departments of Medicine and of Molecular and Cellular Engineering, University of Pennsylvania, and The Wistar Institute, Philadelphia, Pennsylvania 19104, USA. | lld:pubmed |
pubmed-article:10933709 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:10933709 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:10933709 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
entrez-gene:21947 | entrezgene:pubmed | pubmed-article:10933709 | lld:entrezgene |
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