| pubmed-article:12047749 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12047749 | lifeskim:mentions | umls-concept:C0014834 | lld:lifeskim |
| pubmed-article:12047749 | lifeskim:mentions | umls-concept:C0017337 | lld:lifeskim |
| pubmed-article:12047749 | lifeskim:mentions | umls-concept:C1442161 | lld:lifeskim |
| pubmed-article:12047749 | lifeskim:mentions | umls-concept:C0175727 | lld:lifeskim |
| pubmed-article:12047749 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:12047749 | pubmed:dateCreated | 2002-6-5 | lld:pubmed |
| pubmed-article:12047749 | pubmed:abstractText | Activation of human Vgamma9/Vdelta2 T cells by many pathogens depends on the presence of small phosphorylated non-peptide compounds derived from the 2-C-methyl-d-erythritol 4-phosphate (MEP) pathway of isoprenoid biosynthesis. We here demonstrate that in Escherichia coli mutants deficient in lytB, an essential gene of the MEP pathway, a potent Vgamma9/Vdelta2 T-cell activator accumulates by a factor of approximately 150 compared to wild-type E. coli. The compound responsible for the strong immunogenicity of this E. coli mutant was subsequently characterized and identified as a small pyrophosphorylated metabolite, with a molecular mass of 262 Da, derived from the MEP pathway. Stimulation of human peripheral blood mononuclear cells (PBMC) with extracts prepared from the lytB-deficient E. coli mutant led to upregulation of T-cell activation markers on the surface of Vgamma9/Vdelta2 T cells as well as proliferation and expansion of Vgamma9/Vdelta2 T cells. This response was dependent on costimulatory growth factors, such as interleukin (IL)-2, IL-15 and IL-21. Significant levels of interferon-gamma (IFN-gamma) and tumour necrosis factor-alpha (TNF-alpha) were secreted in the presence of IL-2 and IL-15, but not in the presence of IL-21, demonstrating that proliferating phosphoantigen-reactive Vgamma9/Vdelta2 T cells do not necessarily produce proinflammatory cytokines. | lld:pubmed |
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| pubmed-article:12047749 | pubmed:language | eng | lld:pubmed |
| pubmed-article:12047749 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12047749 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:12047749 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12047749 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:12047749 | pubmed:issn | 0019-2805 | lld:pubmed |
| pubmed-article:12047749 | pubmed:author | pubmed-author:WiesnerJochen... | lld:pubmed |
| pubmed-article:12047749 | pubmed:author | pubmed-author:JomaaHassanH | lld:pubmed |
| pubmed-article:12047749 | pubmed:author | pubmed-author:SanderbrandSi... | lld:pubmed |
| pubmed-article:12047749 | pubmed:author | pubmed-author:BeckEwaldE | lld:pubmed |
| pubmed-article:12047749 | pubmed:author | pubmed-author:HintzMartinM | lld:pubmed |
| pubmed-article:12047749 | pubmed:author | pubmed-author:EberlMatthias... | lld:pubmed |
| pubmed-article:12047749 | pubmed:author | pubmed-author:AltincicekBor... | lld:pubmed |
| pubmed-article:12047749 | pubmed:author | pubmed-author:KollasAnn-Kri... | lld:pubmed |
| pubmed-article:12047749 | pubmed:author | pubmed-author:BahrUteU | lld:pubmed |
| pubmed-article:12047749 | pubmed:author | pubmed-author:ReichenbergAr... | lld:pubmed |
| pubmed-article:12047749 | pubmed:author | pubmed-author:FosterDonaldD | lld:pubmed |
| pubmed-article:12047749 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12047749 | pubmed:volume | 106 | lld:pubmed |
| pubmed-article:12047749 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12047749 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12047749 | pubmed:pagination | 200-11 | lld:pubmed |
| pubmed-article:12047749 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
| pubmed-article:12047749 | pubmed:meshHeading | pubmed-meshheading:12047749... | lld:pubmed |
| pubmed-article:12047749 | pubmed:meshHeading | pubmed-meshheading:12047749... | lld:pubmed |
| pubmed-article:12047749 | pubmed:meshHeading | pubmed-meshheading:12047749... | lld:pubmed |
