| pubmed-article:18154620 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18154620 | lifeskim:mentions | umls-concept:C0020792 | lld:lifeskim |
| pubmed-article:18154620 | lifeskim:mentions | umls-concept:C2350466 | lld:lifeskim |
| pubmed-article:18154620 | lifeskim:mentions | umls-concept:C0023688 | lld:lifeskim |
| pubmed-article:18154620 | lifeskim:mentions | umls-concept:C0061105 | lld:lifeskim |
| pubmed-article:18154620 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
| pubmed-article:18154620 | lifeskim:mentions | umls-concept:C0037791 | lld:lifeskim |
| pubmed-article:18154620 | lifeskim:mentions | umls-concept:C0205232 | lld:lifeskim |
| pubmed-article:18154620 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:18154620 | pubmed:dateCreated | 2007-12-24 | lld:pubmed |
| pubmed-article:18154620 | pubmed:abstractText | GD3, a ganglioside expressed on melanoma, is the only tumour-associated glycolipid described to date that can induce a CD1d-restricted natural killer T (NKT)-cell response. We analysed the fine specificity of GD3-reactive NKT cells and discovered that immunization with GD3 induced two populations of GD3-reactive NKT cells. One population was CD4+ CD8- and was specific for GD3; the other population was CD4- CD8- and cross-reacted with GM3 in a CD1d-restricted manner, but did not cross-react with GM2, GD2, or lactosylceramide. This indicated that the T-cell receptors reacting with GD3 recognize glucose-galactose linked to at least one N-acetyl-neuraminic acid but will not accommodate a terminal N-acetylgalactosamine. Immunization with GM2, GM3, GD2, or lactosylceramide did not induce an NKT-cell response. Coimmunization of GM3-loaded antigen-presenting cells (APCs) with GD3-loaded APCs suppressed the NKT-cell response to GD3 in a CD1d-restricted manner. This suppressive effect was specific for GM3 and was a local effect lasting 2-4 days. In vitro, GM3-loaded APCs also suppressed the interleukin-4 response, but not the interferon-gamma response, of NKT cells to alpha-galactosylceramide. However, there was no effect on the T helper type 2 responses of conventional T cells. We found that this suppression was not mediated by soluble factors. We hypothesize that GM3 induces changes to the APC that lead to suppression of T helper type 2-like NKT-cell responses. | lld:pubmed |
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| pubmed-article:18154620 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:18154620 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:18154620 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18154620 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:18154620 | pubmed:issn | 1365-2567 | lld:pubmed |
| pubmed-article:18154620 | pubmed:author | pubmed-author:SchrantzNicol... | lld:pubmed |
| pubmed-article:18154620 | pubmed:author | pubmed-author:ChapmanPaul... | lld:pubmed |
| pubmed-article:18154620 | pubmed:author | pubmed-author:RagupathiGovi... | lld:pubmed |
| pubmed-article:18154620 | pubmed:author | pubmed-author:WuDianna YDY | lld:pubmed |
| pubmed-article:18154620 | pubmed:author | pubmed-author:PrendesMariaM | lld:pubmed |
| pubmed-article:18154620 | pubmed:author | pubmed-author:LuSharon XSX | lld:pubmed |
| pubmed-article:18154620 | pubmed:author | pubmed-author:ParkJun-EuiJE | lld:pubmed |
| pubmed-article:18154620 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:18154620 | pubmed:volume | 123 | lld:pubmed |
| pubmed-article:18154620 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18154620 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18154620 | pubmed:pagination | 145-55 | lld:pubmed |
| pubmed-article:18154620 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:18154620 | pubmed:year | 2008 | lld:pubmed |
| pubmed-article:18154620 | pubmed:articleTitle | Fine specificity of natural killer T cells against GD3 ganglioside and identification of GM3 as an inhibitory natural killer T-cell ligand. | lld:pubmed |
| pubmed-article:18154620 | pubmed:affiliation | Department of Medicine, Swim Across America Laboratory, Memorial Sloan-Kettering Cancer Center, New York, NY 10021, USA. | lld:pubmed |
| pubmed-article:18154620 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:18154620 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:18154620 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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