| pubmed-article:20181652 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20181652 | lifeskim:mentions | umls-concept:C2350466 | lld:lifeskim |
| pubmed-article:20181652 | lifeskim:mentions | umls-concept:C0023688 | lld:lifeskim |
| pubmed-article:20181652 | lifeskim:mentions | umls-concept:C1327413 | lld:lifeskim |
| pubmed-article:20181652 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:20181652 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:20181652 | pubmed:dateCreated | 2010-3-26 | lld:pubmed |
| pubmed-article:20181652 | pubmed:abstractText | NKT cells are characterized by their production of both T(h)1 and T(h)2 cytokines immediately after stimulation with alpha-galactosylceramide (alpha-GalCer), which is composed of alpha-galactopyranose linked to ceramide (itself composed of sphingosine and fatty-acyl chains); the chain length of the ceramide varies and this affects the ability of alpha-GalCer to stimulate cytokine production. However, the contribution of its galactopyranose sugar moiety remains unclear. We synthesized alpha-carba-GalCer, which has an alpha-linked carba-galactosyl moiety; here, the 5a'-oxygen atom of the D-galactopyranose ring of alpha-GalCer is replaced by a methylene group. The alpha-carba-GalCer was more stable and showed higher affinity to the NKT receptor. It thus enhanced and prolonged production of IL-12 and IFN-gamma compared with alpha-GalCer, resulting in augmented NKT cell-mediated adjuvant effects in vivo. The alpha-carba-GalCer, which has an ether linkage, was more resistant to degradation by liver microsomes than was alpha-GalCer, which has an acetal bond. Modulation of the sugar moiety in glycolipids might therefore provide optimal therapeutic reagents for protective immune responses against tumor or pathogens. | lld:pubmed |
| pubmed-article:20181652 | pubmed:language | eng | lld:pubmed |
| pubmed-article:20181652 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20181652 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:20181652 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20181652 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20181652 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20181652 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20181652 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20181652 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20181652 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:20181652 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:20181652 | pubmed:issn | 1460-2377 | lld:pubmed |
| pubmed-article:20181652 | pubmed:author | pubmed-author:TaniguchiMasa... | lld:pubmed |
| pubmed-article:20181652 | pubmed:author | pubmed-author:SumidaTakayuk... | lld:pubmed |
| pubmed-article:20181652 | pubmed:author | pubmed-author:MoriKenjiK | lld:pubmed |
| pubmed-article:20181652 | pubmed:author | pubmed-author:WataraiHirosh... | lld:pubmed |
| pubmed-article:20181652 | pubmed:author | pubmed-author:ChibaTomokiT | lld:pubmed |
| pubmed-article:20181652 | pubmed:author | pubmed-author:ShimizuKanako... | lld:pubmed |
| pubmed-article:20181652 | pubmed:author | pubmed-author:NakagawaRyusu... | lld:pubmed |
| pubmed-article:20181652 | pubmed:author | pubmed-author:FujiiShin-Ich... | lld:pubmed |
| pubmed-article:20181652 | pubmed:author | pubmed-author:ShigeuraTomok... | lld:pubmed |
| pubmed-article:20181652 | pubmed:author | pubmed-author:TashiroTakuya... | lld:pubmed |
| pubmed-article:20181652 | pubmed:author | pubmed-author:InoueSayoS | lld:pubmed |
| pubmed-article:20181652 | pubmed:author | pubmed-author:HongoNaomiN | lld:pubmed |
| pubmed-article:20181652 | pubmed:author | pubmed-author:Omori-MiyakeM... | lld:pubmed |
| pubmed-article:20181652 | pubmed:author | pubmed-author:YoshigaYoheiY | lld:pubmed |
| pubmed-article:20181652 | pubmed:author | pubmed-author:Sekine-KondoE... | lld:pubmed |
| pubmed-article:20181652 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:20181652 | pubmed:volume | 22 | lld:pubmed |
| pubmed-article:20181652 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:20181652 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:20181652 | pubmed:pagination | 319-28 | lld:pubmed |
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| pubmed-article:20181652 | pubmed:meshHeading | pubmed-meshheading:20181652... | lld:pubmed |
| pubmed-article:20181652 | pubmed:year | 2010 | lld:pubmed |
| pubmed-article:20181652 | pubmed:articleTitle | Induction of Th1-biased cytokine production by alpha-carba-GalCer, a neoglycolipid ligand for NKT cells. | lld:pubmed |
| pubmed-article:20181652 | pubmed:affiliation | Laboratory for Immune Regulation, RIKEN Research Center for Allergy and Immunology, Tsurumi, Yokohama, Japan. | lld:pubmed |
| pubmed-article:20181652 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:20181652 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
