| pubmed-article:11312250 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11312250 | lifeskim:mentions | umls-concept:C0027651 | lld:lifeskim |
| pubmed-article:11312250 | lifeskim:mentions | umls-concept:C0030956 | lld:lifeskim |
| pubmed-article:11312250 | lifeskim:mentions | umls-concept:C0035015 | lld:lifeskim |
| pubmed-article:11312250 | lifeskim:mentions | umls-concept:C0042196 | lld:lifeskim |
| pubmed-article:11312250 | lifeskim:mentions | umls-concept:C1444748 | lld:lifeskim |
| pubmed-article:11312250 | lifeskim:mentions | umls-concept:C1707940 | lld:lifeskim |
| pubmed-article:11312250 | lifeskim:mentions | umls-concept:C0456387 | lld:lifeskim |
| pubmed-article:11312250 | lifeskim:mentions | umls-concept:C1882923 | lld:lifeskim |
| pubmed-article:11312250 | lifeskim:mentions | umls-concept:C1548437 | lld:lifeskim |
| pubmed-article:11312250 | lifeskim:mentions | umls-concept:C0205171 | lld:lifeskim |
| pubmed-article:11312250 | pubmed:issue | 5 | lld:pubmed |
| pubmed-article:11312250 | pubmed:dateCreated | 2001-4-20 | lld:pubmed |
| pubmed-article:11312250 | pubmed:abstractText | Epitope spreading has been best characterized as an exacerbating factor in CD4(+) T cell-dependent autoimmune disease models and is believed to occur via presentation of antigens liberated by tissue destruction initiated by CD4(+) T cells specific for a primary epitope. The growing evidence that exogenous antigens can also be processed and presented by class I MHC molecules has suggested that epitope spreading could occur for CD8(+) cytotoxic T lymphocyte (CTL) responses as well. In the context of anti-tumor immunity, expansion of a CTL response to include secondary epitopes could improve the efficacy of therapeutic vaccines. To determine directly whether epitope spreading can occur during an anti-tumor immune response, two defined class I MHC-binding peptides in the P815 tumor model were utilized. We observed that immunization against the single tumor peptide, P1A, followed by rejection of a P1A(+) tumor, subsequently yielded CTL activity and tumor protection against a P1A(-) tumor variant. P1A immunized mice that subsequently rejected tumor challenge developed CTL against a second defined epitope, P1E. These results indicate that, as for class II-restricted peptides in autoimmune disease, epitope spreading can occur for class I-restricted peptides during tumor rejection. A broadened CTL response may help eliminate outgrowth of antigen-negative tumor variants. | lld:pubmed |
| pubmed-article:11312250 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11312250 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11312250 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:11312250 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:11312250 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11312250 | pubmed:month | May | lld:pubmed |
| pubmed-article:11312250 | pubmed:issn | 0953-8178 | lld:pubmed |
| pubmed-article:11312250 | pubmed:author | pubmed-author:GajewskiT FTF | lld:pubmed |
| pubmed-article:11312250 | pubmed:author | pubmed-author:MarkiewiczM... | lld:pubmed |
| pubmed-article:11312250 | pubmed:author | pubmed-author:AshikariAA | lld:pubmed |
| pubmed-article:11312250 | pubmed:author | pubmed-author:FallarinoFF | lld:pubmed |
| pubmed-article:11312250 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11312250 | pubmed:volume | 13 | lld:pubmed |
| pubmed-article:11312250 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11312250 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11312250 | pubmed:pagination | 625-32 | lld:pubmed |
| pubmed-article:11312250 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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| pubmed-article:11312250 | pubmed:meshHeading | pubmed-meshheading:11312250... | lld:pubmed |
| pubmed-article:11312250 | pubmed:year | 2001 | lld:pubmed |
| pubmed-article:11312250 | pubmed:articleTitle | Epitope spreading upon P815 tumor rejection triggered by vaccination with the single class I MHC-restricted peptide P1A. | lld:pubmed |
| pubmed-article:11312250 | pubmed:affiliation | Department of Pathology, University of Chicago, 5841 South Maryland Avenue, MC2115, Chicago, IL 60637, USA. | lld:pubmed |
| pubmed-article:11312250 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11312250 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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