pubmed-article:20132973 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:20132973 | lifeskim:mentions | umls-concept:C0030705 | lld:lifeskim |
pubmed-article:20132973 | lifeskim:mentions | umls-concept:C0382839 | lld:lifeskim |
pubmed-article:20132973 | lifeskim:mentions | umls-concept:C0567416 | lld:lifeskim |
pubmed-article:20132973 | lifeskim:mentions | umls-concept:C0014518 | lld:lifeskim |
pubmed-article:20132973 | lifeskim:mentions | umls-concept:C0038325 | lld:lifeskim |
pubmed-article:20132973 | lifeskim:mentions | umls-concept:C1416683 | lld:lifeskim |
pubmed-article:20132973 | pubmed:issue | 3 | lld:pubmed |
pubmed-article:20132973 | pubmed:dateCreated | 2010-3-15 | lld:pubmed |
pubmed-article:20132973 | pubmed:abstractText | Toxic epidermal necrolysis (TEN) and Stevens-Johnson syndrome (SJS) are severe, bullous cutaneous diseases with uncertain pathogenesis, although cytotoxic T cells seem to be involved. Natural killer (NK)-like activity has been found in blister infiltrates. Cytotoxic T lymphocytes (CTLs) with NK-like activity (NK-CTLs) have been shown to express T-cell receptors restricted by the HLA-Ib molecule HLA-E. Alternatively, the HLA-E-specific activating receptor CD94/NKG2C can trigger T-cell receptor-independent cytotoxicity in CTLs. | lld:pubmed |
pubmed-article:20132973 | pubmed:language | eng | lld:pubmed |
pubmed-article:20132973 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20132973 | pubmed:citationSubset | AIM | lld:pubmed |
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pubmed-article:20132973 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20132973 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:20132973 | pubmed:month | Mar | lld:pubmed |
pubmed-article:20132973 | pubmed:issn | 1097-6825 | lld:pubmed |
pubmed-article:20132973 | pubmed:author | pubmed-author:BellónTeresaT | lld:pubmed |
pubmed-article:20132973 | pubmed:author | pubmed-author:CabañasRosari... | lld:pubmed |
pubmed-article:20132973 | pubmed:author | pubmed-author:MorelEstherE | lld:pubmed |
pubmed-article:20132973 | pubmed:author | pubmed-author:DíazRosaR | lld:pubmed |
pubmed-article:20132973 | pubmed:author | pubmed-author:FiandorAnaA | lld:pubmed |
pubmed-article:20132973 | pubmed:author | pubmed-author:EscamocheroSa... | lld:pubmed |
pubmed-article:20132973 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:20132973 | pubmed:volume | 125 | lld:pubmed |
pubmed-article:20132973 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:20132973 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:20132973 | pubmed:pagination | 703-10, 710.e1-710.e8 | lld:pubmed |
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pubmed-article:20132973 | pubmed:year | 2010 | lld:pubmed |
pubmed-article:20132973 | pubmed:articleTitle | CD94/NKG2C is a killer effector molecule in patients with Stevens-Johnson syndrome and toxic epidermal necrolysis. | lld:pubmed |
pubmed-article:20132973 | pubmed:affiliation | Research Unit, Hospital Universitario La Paz-FIBHULP, Madrid, Spain. | lld:pubmed |
pubmed-article:20132973 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:20132973 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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