| pubmed-article:20042571 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20042571 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
| pubmed-article:20042571 | lifeskim:mentions | umls-concept:C0037083 | lld:lifeskim |
| pubmed-article:20042571 | lifeskim:mentions | umls-concept:C0441471 | lld:lifeskim |
| pubmed-article:20042571 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
| pubmed-article:20042571 | lifeskim:mentions | umls-concept:C0763286 | lld:lifeskim |
| pubmed-article:20042571 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:20042571 | pubmed:dateCreated | 2010-1-21 | lld:pubmed |
| pubmed-article:20042571 | pubmed:abstractText | Mycolactone is a diffusible lipid toxin produced by Mycobacterium ulcerans, the causative agent of a necrotizing skin disease referred to as Buruli ulcer. Intriguingly, patients with progressive lesions display a systemic suppression of Th1 responses that resolves on surgical excision of infected tissues. In this study, we examined the effects of mycolactone on the functional biology of T cells and identified two mechanisms by which mycolactone suppresses cell responsiveness to antigenic stimulation. At noncytotoxic concentrations, mycolactone blocked the activation-induced production of cytokines by a posttranscriptional, mammalian target of rapamycin, and cellular stress-independent mechanism. In addition, mycolactone triggered the lipid-raft association and activation of the Src-family kinase, Lck. Mycolactone-mediated hyperactivation of Lck resulted in the depletion of intracellular calcium stores and downregulation of the TCR, leading to impaired T cell responsiveness to stimulation. These biochemical alterations were not observed when T cells were exposed to other bacterial lipids, or to structurally related immunosuppressors. Mycolactone thus constitutes a novel type of T cell immunosuppressive agent, the potent activity of which may explain the defective cellular responses in Buruli ulcer patients. | lld:pubmed |
| pubmed-article:20042571 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20042571 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20042571 | pubmed:language | eng | lld:pubmed |
| pubmed-article:20042571 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20042571 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:20042571 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20042571 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20042571 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20042571 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20042571 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:20042571 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:20042571 | pubmed:issn | 1550-6606 | lld:pubmed |
| pubmed-article:20042571 | pubmed:author | pubmed-author:BismuthGeorge... | lld:pubmed |
| pubmed-article:20042571 | pubmed:author | pubmed-author:Di... | lld:pubmed |
| pubmed-article:20042571 | pubmed:author | pubmed-author:LangsleyGordo... | lld:pubmed |
| pubmed-article:20042571 | pubmed:author | pubmed-author:DemangelCarol... | lld:pubmed |
| pubmed-article:20042571 | pubmed:author | pubmed-author:BoulkrounShee... | lld:pubmed |
| pubmed-article:20042571 | pubmed:author | pubmed-author:MerckxAnaïsA | lld:pubmed |
| pubmed-article:20042571 | pubmed:author | pubmed-author:ThoulouzeMari... | lld:pubmed |
| pubmed-article:20042571 | pubmed:author | pubmed-author:MonotMarcM | lld:pubmed |
| pubmed-article:20042571 | pubmed:author | pubmed-author:Guenin-MacéLa... | lld:pubmed |
| pubmed-article:20042571 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:20042571 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:20042571 | pubmed:volume | 184 | lld:pubmed |
| pubmed-article:20042571 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:20042571 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:20042571 | pubmed:pagination | 1436-44 | lld:pubmed |
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| pubmed-article:20042571 | pubmed:meshHeading | pubmed-meshheading:20042571... | lld:pubmed |
| pubmed-article:20042571 | pubmed:meshHeading | pubmed-meshheading:20042571... | lld:pubmed |
| pubmed-article:20042571 | pubmed:year | 2010 | lld:pubmed |
| pubmed-article:20042571 | pubmed:articleTitle | Mycolactone suppresses T cell responsiveness by altering both early signaling and posttranslational events. | lld:pubmed |
| pubmed-article:20042571 | pubmed:affiliation | Unité Postulante Pathogénomique Mycobactérienne Intégrée, Institut Pasteur, Paris, France. | lld:pubmed |
| pubmed-article:20042571 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:20042571 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:20042571 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:20042571 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:20042571 | lld:pubmed |
