pubmed-article:15071185 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:15071185 | lifeskim:mentions | umls-concept:C0011306 | lld:lifeskim |
pubmed-article:15071185 | lifeskim:mentions | umls-concept:C1456820 | lld:lifeskim |
pubmed-article:15071185 | lifeskim:mentions | umls-concept:C1418549 | lld:lifeskim |
pubmed-article:15071185 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
pubmed-article:15071185 | lifeskim:mentions | umls-concept:C1254042 | lld:lifeskim |
pubmed-article:15071185 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
pubmed-article:15071185 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
pubmed-article:15071185 | pubmed:issue | 16 | lld:pubmed |
pubmed-article:15071185 | pubmed:dateCreated | 2004-4-21 | lld:pubmed |
pubmed-article:15071185 | pubmed:abstractText | Systemic administration of adenovirus and adenovirus vectors induces a robust innate and adaptive immune response in a variety of animal models. In tumor necrosis factor (TNF)(-/-) mice, a diminished immune response to adenovirus (Ad) infection has been attributed to compromised dendritic cell (DC) maturation. In this report, we investigated the mechanisms responsible for Ad-mediated activation and maturation of DC. Ad infection induced high levels of TNF-alpha expression by murine bone marrow-derived DC, comparable to levels observed with lipopolysaccharide exposure. Ad-induced TNF-alpha production was necessary for DC maturation and acts in an autocrine manner. Unlike TNF-alpha production associated with exposure to lipopolysaccharide, Ad induction of TNF-alpha was not dependent on the MyD88 signaling pathway. In contrast, Ad-induced TNF-alpha production and DC maturation were dependent on signaling by phosphoinositide-3-OH kinase (PI3K), as determined by wortmannin and LY294002 blocking experiments. The adenovirus capsid protein penton contains a well characterized arginine-glycine-aspartic acid integrin-binding domain that stimulates PI3K in fibroblast cell lines. When this region of the penton was mutated, TNF-alpha expression and bone marrow-derived DC maturation were attenuated. We propose that integrin-mediated PI3K induction of NF-kappaB activates an autocrine TNF-alpha pathway required for DC maturation in response to Ad. | lld:pubmed |
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pubmed-article:15071185 | pubmed:language | eng | lld:pubmed |
pubmed-article:15071185 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15071185 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:15071185 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:15071185 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:15071185 | pubmed:month | Apr | lld:pubmed |
pubmed-article:15071185 | pubmed:issn | 0027-8424 | lld:pubmed |
pubmed-article:15071185 | pubmed:author | pubmed-author:PhilpottNicol... | lld:pubmed |
pubmed-article:15071185 | pubmed:author | pubmed-author:Falck-Pederse... | lld:pubmed |
pubmed-article:15071185 | pubmed:author | pubmed-author:ElkonKeith... | lld:pubmed |
pubmed-article:15071185 | pubmed:author | pubmed-author:NociariMarcel... | lld:pubmed |
pubmed-article:15071185 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:15071185 | pubmed:day | 20 | lld:pubmed |
pubmed-article:15071185 | pubmed:volume | 101 | lld:pubmed |
pubmed-article:15071185 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:15071185 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:15071185 | pubmed:pagination | 6200-5 | lld:pubmed |
pubmed-article:15071185 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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