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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
5
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pubmed:dateCreated |
1997-3-11
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pubmed:abstractText |
The B7 family of costimulatory molecules provides the second signal necessary for activation of T cells. In the absence of the second signal, responding T cells become anergic. Although predominantly expressed on professional APCs, recent evidence shows that the B7 molecules are also expressed on T cells. To study the functions of B7 molecules on T cells, we transfected murine B7.1 (CD80) and B7.2 (CD86) cDNAs into the EL4 T cell thymoma cell line and examined the transfectants for their ability to costimulate T cell proliferation in vitro and to induce antitumor immunity in vivo. Here we show that although EL4-B7.1 cells costimulate T cells and induce tumor regression, EL4-B7.2 transfectants failed to costimulate T cell proliferation or induce tumor regression. To understand the cellular basis for this difference, we examined the binding of EL4-B7.1 and EL4-B7.2 to CTLA4 and CD28. Whereas EL4-B7.1 cells bound both CTLA4-Ig and CD28-Ig, EL4-B7.2 transfectants preferentially bound CTLA4-Ig, but not CD28-Ig. Similar binding data were obtained with freshly isolated murine T cells, which have been shown to constitutively express B7.2. Our data suggest, therefore, that B7.2 expressed on T cells may not costimulate but instead inhibit the T cell response by preferential binding to CTLA4.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD28,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD86,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Differentiation,
http://linkedlifedata.com/resource/pubmed/chemical/CTLA-4 Antigen,
http://linkedlifedata.com/resource/pubmed/chemical/Cd86 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Ctla4 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoconjugates,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/abatacept
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0022-1767
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pubmed:author |
pubmed-author:BenazzoFF,
pubmed-author:DavisGG,
pubmed-author:FreemanG JGJ,
pubmed-author:GreenfieldE AEA,
pubmed-author:HöllsbergPP,
pubmed-author:HaflerD ADA,
pubmed-author:HowardEE,
pubmed-author:KuchrooV KVK,
pubmed-author:McLeanPP,
pubmed-author:NguyenKK,
pubmed-author:ParadisTT,
pubmed-author:SharpeA HAH
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pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
158
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2025-34
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:9036945-Animals,
pubmed-meshheading:9036945-Antigens, CD,
pubmed-meshheading:9036945-Antigens, CD28,
pubmed-meshheading:9036945-Antigens, CD86,
pubmed-meshheading:9036945-Antigens, Differentiation,
pubmed-meshheading:9036945-CTLA-4 Antigen,
pubmed-meshheading:9036945-Cell Division,
pubmed-meshheading:9036945-Female,
pubmed-meshheading:9036945-Immunoconjugates,
pubmed-meshheading:9036945-Lymphocyte Activation,
pubmed-meshheading:9036945-Membrane Glycoproteins,
pubmed-meshheading:9036945-Mice,
pubmed-meshheading:9036945-Mice, Inbred BALB C,
pubmed-meshheading:9036945-Mice, Inbred C57BL,
pubmed-meshheading:9036945-Protein Binding,
pubmed-meshheading:9036945-T-Lymphocytes,
pubmed-meshheading:9036945-Thymoma,
pubmed-meshheading:9036945-Thymus Neoplasms,
pubmed-meshheading:9036945-Transfection,
pubmed-meshheading:9036945-Tumor Cells, Cultured
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pubmed:year |
1997
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pubmed:articleTitle |
B7.2 expressed by T cells does not induce CD28-mediated costimulatory activity but retains CTLA4 binding: implications for induction of antitumor immunity to T cell tumors.
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pubmed:affiliation |
Division of Hematologic Malignancies, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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