| 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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MedLine Citation:
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PMID: 9036945 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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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Authors:
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E A Greenfield; E Howard; T Paradis; K Nguyen; F Benazzo; P McLean; P Höllsberg; G Davis; D A Hafler; A H Sharpe; G J Freeman; V K Kuchroo |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Journal of immunology (Baltimore, Md. : 1950) Volume: 158 ISSN: 0022-1767 ISO Abbreviation: J. Immunol. Publication Date: 1997 Mar |
Date Detail:
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Created Date: 1997-03-11 Completed Date: 1997-03-11 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 2985117R Medline TA: J Immunol Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 2025-34 Citation Subset: AIM; IM |
Affiliation:
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Division of Hematologic Malignancies, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Antigens, CD / biosynthesis*, metabolism, pharmacology* Antigens, CD28 / metabolism, physiology* Antigens, CD86 Antigens, Differentiation / metabolism* Cell Division Female Immunoconjugates* Lymphocyte Activation* Membrane Glycoproteins / biosynthesis*, metabolism, pharmacology* Mice Mice, Inbred BALB C Mice, Inbred C57BL Protein Binding / immunology T-Lymphocytes / immunology, metabolism* Thymoma / immunology*, prevention & control Thymus Neoplasms / immunology*, prevention & control Transfection / immunology Tumor Cells, Cultured |
| Grant Support | |
ID/Acronym/Agency:
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NS 30843/NS/NINDS NIH HHS; P01 AR43220/AR/NIAMS NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Antigens, CD; 0/Antigens, CD28; 0/Antigens, CD86; 0/Antigens, Differentiation; 0/Cd86 protein, mouse; 0/Immunoconjugates; 0/Membrane Glycoproteins; 0/abatacept; 0/cytotoxic T-lymphocyte antigen 4 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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