| pubmed-article:10629086 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10629086 | lifeskim:mentions | umls-concept:C0025202 | lld:lifeskim |
| pubmed-article:10629086 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
| pubmed-article:10629086 | lifeskim:mentions | umls-concept:C1522642 | lld:lifeskim |
| pubmed-article:10629086 | lifeskim:mentions | umls-concept:C1513095 | lld:lifeskim |
| pubmed-article:10629086 | lifeskim:mentions | umls-concept:C0019721 | lld:lifeskim |
| pubmed-article:10629086 | lifeskim:mentions | umls-concept:C1332714 | lld:lifeskim |
| pubmed-article:10629086 | lifeskim:mentions | umls-concept:C0456387 | lld:lifeskim |
| pubmed-article:10629086 | lifeskim:mentions | umls-concept:C0205225 | lld:lifeskim |
| pubmed-article:10629086 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:10629086 | pubmed:dateCreated | 2000-2-1 | lld:pubmed |
| pubmed-article:10629086 | pubmed:abstractText | The involvement of HLA-class I in target cell lysis by CD4(+) cytolytic T cells (CTL) has been a controversial issue. A CTL clone of CD4 phenotype was derived from the peripheral blood lymphocytes of a patient with primary melanoma. The CTL clone stably lysed the autologous primary melanoma cells for approximately 9 months in culture. Both the Valpha2/Vbeta8 T-cell receptor and CD4 were involved in CTL cytotoxicity. Of a large panel of allogeneic primary and metastatic melanoma or colorectal carcinoma cells, autologous and allogeneic Epstein-Barr virus-transformed B cells and autologous fibroblasts, only allogeneic metastatic melanoma cells matched with the autologous tumor cells for HLA-class I (B57[17]) were lysed and induced IFN-gamma secretion by the CTL clone. Lysis of the autologous tumor cells was significantly blocked by monoclonal antibody to HLA-B17. Importantly, allogeneic, HLA-class I- and class II-unmatched melanoma cells were lysed by the CTL only following transfection of the cells with B57[17] cDNA. Our results provide direct evidence for the involvement of both CD4 and HLA-class I in tumor cell lysis by CD4(+) CTL. | lld:pubmed |
| pubmed-article:10629086 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10629086 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10629086 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10629086 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:10629086 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10629086 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10629086 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10629086 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10629086 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10629086 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10629086 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10629086 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10629086 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:10629086 | pubmed:issn | 0020-7136 | lld:pubmed |
| pubmed-article:10629086 | pubmed:author | pubmed-author:HerlynDD | lld:pubmed |
| pubmed-article:10629086 | pubmed:author | pubmed-author:LomJJ | lld:pubmed |
| pubmed-article:10629086 | pubmed:author | pubmed-author:PatelAA | lld:pubmed |
| pubmed-article:10629086 | pubmed:author | pubmed-author:RobbinsPP | lld:pubmed |
| pubmed-article:10629086 | pubmed:author | pubmed-author:GuerryDD | lld:pubmed |
| pubmed-article:10629086 | pubmed:author | pubmed-author:MarincolaFF | lld:pubmed |
| pubmed-article:10629086 | pubmed:author | pubmed-author:MoonkaDD | lld:pubmed |
| pubmed-article:10629086 | pubmed:author | pubmed-author:SomasundaramR... | lld:pubmed |
| pubmed-article:10629086 | pubmed:copyrightInfo | Copyright 2000 Wiley-Liss, Inc. | lld:pubmed |
| pubmed-article:10629086 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10629086 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:10629086 | pubmed:volume | 85 | lld:pubmed |
| pubmed-article:10629086 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10629086 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10629086 | pubmed:pagination | 253-9 | lld:pubmed |
| pubmed-article:10629086 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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| pubmed-article:10629086 | pubmed:meshHeading | pubmed-meshheading:10629086... | lld:pubmed |
| pubmed-article:10629086 | pubmed:meshHeading | pubmed-meshheading:10629086... | lld:pubmed |
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| pubmed-article:10629086 | pubmed:meshHeading | pubmed-meshheading:10629086... | lld:pubmed |
| pubmed-article:10629086 | pubmed:year | 2000 | lld:pubmed |
| pubmed-article:10629086 | pubmed:articleTitle | CD4(+), HLA class I-restricted, cytolytic T-lymphocyte clone against primary malignant melanoma cells. | lld:pubmed |
| pubmed-article:10629086 | pubmed:affiliation | The Wistar Institute, Philadelphia, PA 19104, USA. | lld:pubmed |
| pubmed-article:10629086 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10629086 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:10629086 | pubmed:publicationType | Case Reports | lld:pubmed |
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