pubmed-article:19433551 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:19433551 | lifeskim:mentions | umls-concept:C0006837 | lld:lifeskim |
pubmed-article:19433551 | lifeskim:mentions | umls-concept:C0011306 | lld:lifeskim |
pubmed-article:19433551 | lifeskim:mentions | umls-concept:C0001128 | lld:lifeskim |
pubmed-article:19433551 | lifeskim:mentions | umls-concept:C0670896 | lld:lifeskim |
pubmed-article:19433551 | lifeskim:mentions | umls-concept:C0439677 | lld:lifeskim |
pubmed-article:19433551 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
pubmed-article:19433551 | pubmed:issue | 7 | lld:pubmed |
pubmed-article:19433551 | pubmed:dateCreated | 2009-6-22 | lld:pubmed |
pubmed-article:19433551 | pubmed:abstractText | The innate immune system of humans recognizes the human pathogenic fungus Candida albicans via sugar polymers present in the cell wall, such as mannan and beta-glucan. Here, we examined whether nucleic acids from C. albicans activate dendritic cells. C. albicans DNA induced interleukin-12p40 (IL-12p40) production and CD40 expression by murine bone marrow-derived myeloid dendritic cells (BM-DCs) in a dose-dependent manner. BM-DCs that lacked Toll-like receptor 4 (TLR4), TLR2, and dectin-1, which are pattern recognition receptors for fungal cell wall components, produced IL-12p40 at levels comparable to the levels produced by BM-DCs from wild-type mice, and DNA from a C. albicans pmr1Delta null mutant, which has a gross defect in mannosylation, retained the ability to activate BM-DCs. This stimulatory effect disappeared completely after DNase treatment. In contrast, RNase treatment increased production of the cytokine. A similar reduction in cytokine production was observed when BM-DCs from TLR9(-/-) and MyD88(-/-) mice were used. In a luciferase reporter assay, NF-kappaB activation was detected in TLR9-expressing HEK293T cells stimulated with C. albicans DNA. Confocal microscopic analysis showed similar localization of C. albicans DNA and CpG-oligodeoxynucleotide (CpG-ODN) in BM-DCs. Treatment of C. albicans DNA with methylase did not affect its ability to induce IL-12p40 synthesis, whereas the same treatment completely eliminated the ability of CpG-ODN to induce IL-12p40 synthesis. Finally, impaired clearance of this fungal pathogen was not found in the kidneys of TLR9(-/-) mice. These results suggested that C. albicans DNA activated BM-DCs through a TLR9-mediated signaling pathway using a mechanism independent of the unmethylated CpG motif. | lld:pubmed |
pubmed-article:19433551 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:19433551 | pubmed:language | eng | lld:pubmed |
pubmed-article:19433551 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19433551 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:19433551 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19433551 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:19433551 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19433551 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:19433551 | pubmed:month | Jul | lld:pubmed |
pubmed-article:19433551 | pubmed:issn | 1098-5522 | lld:pubmed |
pubmed-article:19433551 | pubmed:author | pubmed-author:IwakuraYoichi... | lld:pubmed |
pubmed-article:19433551 | pubmed:author | pubmed-author:TakedaKiyoshi... | lld:pubmed |
pubmed-article:19433551 | pubmed:author | pubmed-author:AkiraShizuoS | lld:pubmed |
pubmed-article:19433551 | pubmed:author | pubmed-author:OhnoNaohitoN | lld:pubmed |
pubmed-article:19433551 | pubmed:author | pubmed-author:AdachiYoshiyu... | lld:pubmed |
pubmed-article:19433551 | pubmed:author | pubmed-author:SaijoShinobuS | lld:pubmed |
pubmed-article:19433551 | pubmed:author | pubmed-author:KawakamiKazuy... | lld:pubmed |
pubmed-article:19433551 | pubmed:author | pubmed-author:KakuMitsuoM | lld:pubmed |
pubmed-article:19433551 | pubmed:author | pubmed-author:IshiiKeikoK | lld:pubmed |
pubmed-article:19433551 | pubmed:author | pubmed-author:MiyazatoAkiko... | lld:pubmed |
pubmed-article:19433551 | pubmed:author | pubmed-author:YamamotoNatsu... | lld:pubmed |
pubmed-article:19433551 | pubmed:author | pubmed-author:GowNeil A RNA | lld:pubmed |
pubmed-article:19433551 | pubmed:author | pubmed-author:MitsutakeKota... | lld:pubmed |
pubmed-article:19433551 | pubmed:author | pubmed-author:TanakaMisuzuM | lld:pubmed |
pubmed-article:19433551 | pubmed:author | pubmed-author:XiaoGangG | lld:pubmed |
pubmed-article:19433551 | pubmed:author | pubmed-author:AbeYuzuruY | lld:pubmed |
pubmed-article:19433551 | pubmed:author | pubmed-author:Mora-MontesHé... | lld:pubmed |
pubmed-article:19433551 | pubmed:author | pubmed-author:IndenKenK | lld:pubmed |
pubmed-article:19433551 | pubmed:author | pubmed-author:NakamuraKiwam... | lld:pubmed |
pubmed-article:19433551 | pubmed:author | pubmed-author:TannoDaikiD | lld:pubmed |
pubmed-article:19433551 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:19433551 | pubmed:volume | 77 | lld:pubmed |
pubmed-article:19433551 | pubmed:owner | NLM | lld:pubmed |