Source:http://linkedlifedata.com/resource/pubmed/id/15472713
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2
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| pubmed:dateCreated |
2005-1-19
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| pubmed:abstractText |
Recent evidence has resurrected the concept of specialized populations of T lymphocytes that are able to suppress an antigen-specific immune response. T-regulatory cells (T-reg) have been characterized as CD4+ CD25+ T cells. Previous reports describing differential gene expression analysis have shown that the glucocorticoid-induced tumor necrosis family receptor family-related gene (GITR) is upregulated in these cells. Furthermore, antibodies specific for GITR have been shown to inhibit the T-suppressor function of CD4+ CD25+ T-reg. The ligands for both mouse and human GITR have been cloned recently. We have inserted the sequences for natural, membrane-bound GITR-ligand (GITR-L) and a truncated secreted form of GITR-L (GITR-Lsol) into the adenovirus-5 genome. Coculture experiments show that cells infected with Ad-GITR-L and supernatants from cells infected with Ad-GITR-Lsol can increase the proliferation of both CD4+ CD25- and CD8+ T cells in response to anti-CD3 stimulation, in the presence, as well as in the absence, of CD4+ CD25+ T cells. The virus constructs were injected into growing B16 melanoma tumors. Ad-GITR-L was shown to attract infiltration with both CD4+ and CD8+ T cells. Both constructs were shown to inhibit tumor growth.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD28,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD4,
http://linkedlifedata.com/resource/pubmed/chemical/Carrier Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Ligands,
http://linkedlifedata.com/resource/pubmed/chemical/Tnfsf18 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factors
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| pubmed:status |
MEDLINE
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| pubmed:month |
Feb
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| pubmed:issn |
0929-1903
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
12
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
198-205
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| pubmed:dateRevised |
2006-11-15
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| pubmed:meshHeading |
pubmed-meshheading:15472713-Adenoviridae,
pubmed-meshheading:15472713-Animals,
pubmed-meshheading:15472713-Antigens, CD28,
pubmed-meshheading:15472713-Antigens, CD4,
pubmed-meshheading:15472713-CD4-Positive T-Lymphocytes,
pubmed-meshheading:15472713-Carrier Proteins,
pubmed-meshheading:15472713-Cell Membrane,
pubmed-meshheading:15472713-Cell Proliferation,
pubmed-meshheading:15472713-Coculture Techniques,
pubmed-meshheading:15472713-Female,
pubmed-meshheading:15472713-Immunosuppression,
pubmed-meshheading:15472713-Ligands,
pubmed-meshheading:15472713-Melanoma, Experimental,
pubmed-meshheading:15472713-Mice,
pubmed-meshheading:15472713-Mice, Inbred C57BL,
pubmed-meshheading:15472713-Plasmids,
pubmed-meshheading:15472713-T-Lymphocytes, Regulatory,
pubmed-meshheading:15472713-Tumor Necrosis Factors
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| pubmed:year |
2005
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| pubmed:articleTitle |
Bypassing tumor-associated immune suppression with recombinant adenovirus constructs expressing membrane bound or secreted GITR-L.
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| pubmed:affiliation |
Molecular Immunology Laboratory, Transgene SA, Strasbourg 67082, France. calmels@transgene.fr
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| pubmed:publicationType |
Journal Article
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