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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
19
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pubmed:dateCreated |
2002-9-18
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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.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/12218188-10485649,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12218188-10823416,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12218188-11015443,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12218188-11209085,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12218188-11224527,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12218188-11244047,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12218188-11323285,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12218188-11343123,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12218188-11673519,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12218188-12161284,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12218188-1903428,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12218188-7481803,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12218188-7513904,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12218188-7594546,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12218188-8011285,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12218188-8596936,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12218188-8671665,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12218188-8752916,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12218188-9010723,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12218188-9136454,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12218188-9269687,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12218188-9354465,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12218188-9796923,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12218188-9862337
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Monoclonal,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD274,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD80,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Surface,
http://linkedlifedata.com/resource/pubmed/chemical/Apoptosis Regulatory Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Blood Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Cd274 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Pdcd1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Peptides,
http://linkedlifedata.com/resource/pubmed/chemical/Programmed Cell Death 1 Receptor,
http://linkedlifedata.com/resource/pubmed/chemical/Proteins
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0027-8424
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
17
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pubmed:volume |
99
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
12293-7
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:12218188-Animals,
pubmed-meshheading:12218188-Antibodies, Monoclonal,
pubmed-meshheading:12218188-Antigens, CD274,
pubmed-meshheading:12218188-Antigens, CD80,
pubmed-meshheading:12218188-Antigens, Surface,
pubmed-meshheading:12218188-Apoptosis Regulatory Proteins,
pubmed-meshheading:12218188-Blood Proteins,
pubmed-meshheading:12218188-Immunotherapy,
pubmed-meshheading:12218188-Membrane Glycoproteins,
pubmed-meshheading:12218188-Mice,
pubmed-meshheading:12218188-Mice, Inbred BALB C,
pubmed-meshheading:12218188-Mice, Inbred C57BL,
pubmed-meshheading:12218188-Mice, Inbred DBA,
pubmed-meshheading:12218188-Mice, Knockout,
pubmed-meshheading:12218188-Mice, Nude,
pubmed-meshheading:12218188-Multiple Myeloma,
pubmed-meshheading:12218188-Neoplasms, Experimental,
pubmed-meshheading:12218188-Peptides,
pubmed-meshheading:12218188-Programmed Cell Death 1 Receptor,
pubmed-meshheading:12218188-Proteins,
pubmed-meshheading:12218188-Self Tolerance,
pubmed-meshheading:12218188-T-Lymphocytes, Cytotoxic,
pubmed-meshheading:12218188-Transfection,
pubmed-meshheading:12218188-Tumor Cells, Cultured
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pubmed:year |
2002
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pubmed:articleTitle |
Involvement of PD-L1 on tumor cells in the escape from host immune system and tumor immunotherapy by PD-L1 blockade.
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pubmed:affiliation |
Department of Medical Chemistry, Graduate School of Medicine, Japan Science and Technology Corporation, Kyoto 606-8501, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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