| pubmed-article:12218188 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12218188 | lifeskim:mentions | umls-concept:C0027651 | lld:lifeskim |
| pubmed-article:12218188 | lifeskim:mentions | umls-concept:C0020962 | lld:lifeskim |
| pubmed-article:12218188 | lifeskim:mentions | umls-concept:C0021083 | lld:lifeskim |
| pubmed-article:12218188 | lifeskim:mentions | umls-concept:C1167395 | lld:lifeskim |
| pubmed-article:12218188 | lifeskim:mentions | umls-concept:C0431085 | lld:lifeskim |
| pubmed-article:12218188 | lifeskim:mentions | umls-concept:C1540292 | lld:lifeskim |
| pubmed-article:12218188 | lifeskim:mentions | umls-concept:C1314939 | lld:lifeskim |
| pubmed-article:12218188 | lifeskim:mentions | umls-concept:C0332206 | lld:lifeskim |
| pubmed-article:12218188 | lifeskim:mentions | umls-concept:C0870509 | lld:lifeskim |
| pubmed-article:12218188 | pubmed:issue | 19 | lld:pubmed |
| pubmed-article:12218188 | pubmed:dateCreated | 2002-9-18 | lld:pubmed |
| pubmed-article:12218188 | pubmed:abstractText | PD-1 is a receptor of the Ig superfamily that negatively regulates T cell antigen receptor signaling by interacting with the specific ligands (PD-L) and is suggested to play a role in the maintenance of self-tolerance. In the present study, we examined possible roles of the PD-1/PD-L system in tumor immunity. Transgenic expression of PD-L1, one of the PD-L, in P815 tumor cells rendered them less susceptible to the specific T cell antigen receptor-mediated lysis by cytotoxic T cells in vitro, and markedly enhanced their tumorigenesis and invasiveness in vivo in the syngeneic hosts as compared with the parental tumor cells that lacked endogenous PD-L. Both effects could be reversed by anti-PD-L1 Ab. Survey of murine tumor lines revealed that all of the myeloma cell lines examined naturally expressed PD-L1. Growth of the myeloma cells in normal syngeneic mice was inhibited significantly albeit transiently by the administration of anti-PD-L1 Ab in vivo and was suppressed completely in the syngeneic PD-1-deficient mice. These results suggest that the expression of PD-L1 can serve as a potent mechanism for potentially immunogenic tumors to escape from host immune responses and that blockade of interaction between PD-1 and PD-L may provide a promising strategy for specific tumor immunotherapy. | lld:pubmed |
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| pubmed-article:12218188 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:12218188 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:12218188 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12218188 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:12218188 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:12218188 | pubmed:author | pubmed-author:HonjoTasukuT | lld:pubmed |
| pubmed-article:12218188 | pubmed:author | pubmed-author:TanakaYoshima... | lld:pubmed |
| pubmed-article:12218188 | pubmed:author | pubmed-author:MinatoNagahir... | lld:pubmed |
| pubmed-article:12218188 | pubmed:author | pubmed-author:OkazakiTakuT | lld:pubmed |
| pubmed-article:12218188 | pubmed:author | pubmed-author:IwaiYoshikoY | lld:pubmed |
| pubmed-article:12218188 | pubmed:author | pubmed-author:IshidaMasayos... | lld:pubmed |
| pubmed-article:12218188 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12218188 | pubmed:day | 17 | lld:pubmed |
| pubmed-article:12218188 | pubmed:volume | 99 | lld:pubmed |
| pubmed-article:12218188 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12218188 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12218188 | pubmed:pagination | 12293-7 | lld:pubmed |
| pubmed-article:12218188 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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| pubmed-article:12218188 | pubmed:year | 2002 | lld:pubmed |
| pubmed-article:12218188 | pubmed:articleTitle | Involvement of PD-L1 on tumor cells in the escape from host immune system and tumor immunotherapy by PD-L1 blockade. | lld:pubmed |
| pubmed-article:12218188 | pubmed:affiliation | Department of Medical Chemistry, Graduate School of Medicine, Japan Science and Technology Corporation, Kyoto 606-8501, Japan. | lld:pubmed |
| pubmed-article:12218188 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:12218188 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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