pubmed-article:16148096 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:16148096 | lifeskim:mentions | umls-concept:C1332717 | lld:lifeskim |
pubmed-article:16148096 | lifeskim:mentions | umls-concept:C1706438 | lld:lifeskim |
pubmed-article:16148096 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
pubmed-article:16148096 | lifeskim:mentions | umls-concept:C0085358 | lld:lifeskim |
pubmed-article:16148096 | lifeskim:mentions | umls-concept:C0546816 | lld:lifeskim |
pubmed-article:16148096 | lifeskim:mentions | umls-concept:C0033414 | lld:lifeskim |
pubmed-article:16148096 | lifeskim:mentions | umls-concept:C0041361 | lld:lifeskim |
pubmed-article:16148096 | lifeskim:mentions | umls-concept:C1332397 | lld:lifeskim |
pubmed-article:16148096 | lifeskim:mentions | umls-concept:C1413244 | lld:lifeskim |
pubmed-article:16148096 | lifeskim:mentions | umls-concept:C2698600 | lld:lifeskim |
pubmed-article:16148096 | lifeskim:mentions | umls-concept:C1420812 | lld:lifeskim |
pubmed-article:16148096 | lifeskim:mentions | umls-concept:C1705180 | lld:lifeskim |
pubmed-article:16148096 | pubmed:issue | 6 | lld:pubmed |
pubmed-article:16148096 | pubmed:dateCreated | 2005-9-8 | lld:pubmed |
pubmed-article:16148096 | pubmed:abstractText | The molecular signals that allow primed CD8 T cells to persist and be effective are particularly important during cancer growth. With response to tumor-expressed Ag following adoptive T cell transfer, we show that CD8 effector cells deficient in OX40, a TNFR family member, could not mediate short-term tumor suppression. OX40 was required at two critical stages. The first was during CD8 priming in vitro, in which APC-transmitted OX40 signals endowed the ability to survive when adoptively transferred in vivo before tumor Ag encounter. The second was during the in vivo recall response of primed CD8 T cells, the stage in which OX40 contributed to the further survival and accumulation of T cells at the tumor site. The lack of OX40 costimulation was associated with reduced levels of Bcl-x(L), and retroviral expression of Bcl-x(L) in tumor-reactive CD8 T cells conferred greatly enhanced tumor protection following adoptive transfer. These data demonstrate that OX40 and Bcl-x(L) can control survival of primed CD8 T cells and provide new insights into both regulation of CD8 immunity and control of tumors. | lld:pubmed |
pubmed-article:16148096 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16148096 | pubmed:language | eng | lld:pubmed |
pubmed-article:16148096 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16148096 | pubmed:citationSubset | AIM | lld:pubmed |
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pubmed-article:16148096 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:16148096 | pubmed:month | Sep | lld:pubmed |
pubmed-article:16148096 | pubmed:issn | 0022-1767 | lld:pubmed |
pubmed-article:16148096 | pubmed:author | pubmed-author:SongAihuaA | lld:pubmed |
pubmed-article:16148096 | pubmed:author | pubmed-author:CroftMichaelM | lld:pubmed |
pubmed-article:16148096 | pubmed:author | pubmed-author:TangXiaohongX | lld:pubmed |
pubmed-article:16148096 | pubmed:author | pubmed-author:HarmsKate... | lld:pubmed |
pubmed-article:16148096 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:16148096 | pubmed:day | 15 | lld:pubmed |
pubmed-article:16148096 | pubmed:volume | 175 | lld:pubmed |
pubmed-article:16148096 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:16148096 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:16148096 | pubmed:pagination | 3534-41 | lld:pubmed |
pubmed-article:16148096 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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pubmed-article:16148096 | pubmed:year | 2005 | lld:pubmed |
pubmed-article:16148096 | pubmed:articleTitle | OX40 and Bcl-xL promote the persistence of CD8 T cells to recall tumor-associated antigen. | lld:pubmed |
pubmed-article:16148096 | pubmed:affiliation | Division of Molecular Immunology, La Jolla Institute for Allergy and Immunology, San Diego, CA 92121, USA. | lld:pubmed |
pubmed-article:16148096 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:16148096 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:16148096 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
pubmed-article:16148096 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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