pubmed-article:12634387 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:12634387 | lifeskim:mentions | umls-concept:C0007600 | lld:lifeskim |
pubmed-article:12634387 | lifeskim:mentions | umls-concept:C0014834 | lld:lifeskim |
pubmed-article:12634387 | lifeskim:mentions | umls-concept:C1332717 | lld:lifeskim |
pubmed-article:12634387 | lifeskim:mentions | umls-concept:C1706438 | lld:lifeskim |
pubmed-article:12634387 | lifeskim:mentions | umls-concept:C0085358 | lld:lifeskim |
pubmed-article:12634387 | lifeskim:mentions | umls-concept:C0014372 | lld:lifeskim |
pubmed-article:12634387 | lifeskim:mentions | umls-concept:C1413244 | lld:lifeskim |
pubmed-article:12634387 | lifeskim:mentions | umls-concept:C2698600 | lld:lifeskim |
pubmed-article:12634387 | lifeskim:mentions | umls-concept:C0162388 | lld:lifeskim |
pubmed-article:12634387 | lifeskim:mentions | umls-concept:C2349975 | lld:lifeskim |
pubmed-article:12634387 | lifeskim:mentions | umls-concept:C1711351 | lld:lifeskim |
pubmed-article:12634387 | pubmed:issue | 7 | lld:pubmed |
pubmed-article:12634387 | pubmed:dateCreated | 2003-3-13 | lld:pubmed |
pubmed-article:12634387 | pubmed:abstractText | Epstein-Barr virus (EBV) is associated with a number of important human cancers, including nasopharyngeal carcinoma, gastric carcinoma, and Hodgkin's lymphoma. These tumors express a viral nuclear antigen, EBV nuclear antigen 1 (EBNA1), which cannot be presented to T cells in a major histocompatibility complex class I context, and the viral latent membrane proteins (LMPs). Although the LMPs are expressed in these tumors, no effective immune response is made. We report here that exposure to the cholera-like enterotoxin B subunit (EtxB) in EBV-infected lymphoblastoid cell lines (LCLs) enhances their susceptibility to killing by LMP-specific CD8(+) cytotoxic T lymphocytes (CTLs) in a HLA class I-restricted manner. CTL killing of LCLs is dramatically increased through both transporter-associated protein-dependent and -independent epitopes after EtxB treatment. The use of mutant B subunits revealed that the enhanced susceptibility of LCLs to CTL killing is dependent on the B subunit's interaction with GM(1) but not its signaling properties. These important findings could underpin the development of novel approaches to treating EBV-associated malignancies and may offer a general approach to increasing the presentation of other tumor and viral antigens. | lld:pubmed |
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pubmed-article:12634387 | pubmed:language | eng | lld:pubmed |
pubmed-article:12634387 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12634387 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:12634387 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:12634387 | pubmed:month | Apr | lld:pubmed |
pubmed-article:12634387 | pubmed:issn | 0022-538X | lld:pubmed |
pubmed-article:12634387 | pubmed:author | pubmed-author:HirstTimothy... | lld:pubmed |
pubmed-article:12634387 | pubmed:author | pubmed-author:WilsonA... | lld:pubmed |
pubmed-article:12634387 | pubmed:author | pubmed-author:MorganAndrew... | lld:pubmed |
pubmed-article:12634387 | pubmed:author | pubmed-author:OngKong-WeeKW | lld:pubmed |
pubmed-article:12634387 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:12634387 | pubmed:volume | 77 | lld:pubmed |
pubmed-article:12634387 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:12634387 | pubmed:authorsComplete | Y | lld:pubmed |