| Overexpression of p65 and c-Jun substitutes for B7-1 costimulation by targeting the CD28RE within the IL-2 promoter. | |
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MedLine Citation:
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PMID: 9605137 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The role of Rel and activation protein-1 (AP-1) in IL-2 promoter activity in B7-1- and leukocyte function-associated Ag-3 (LFA. 3)-costimulated T cells has been evaluated. We demonstrate that overexpression of c-Jun but not c-Fos increases IL-2 promoter activity in both B7-1- and LFA-3-costimulated Jurkat T cells. Cotransfection of both c-Jun and c-Fos substitutes for B7-1 costimulation in driving an activation protein-1 response element but not for the IL-2 promoter. Overexpression of Rel proteins demonstrated that p65-expressing Jurkat cells transcribed equally well a nuclear factor kappabeta reporter construct when costimulated with B7-1 or LFA-3, but transcription of IL-2 promoter or CD28 response element (CD28RE)-driven reporters was superior in B7-1-costimulated cells. Combined expression of c-Jun and p65 induced vigorous transcription of IL-2 promoter- and CD28RE-driven reporter constructs in both LFA-3- and B7-1-costimulated Jurkat cells. Mutating the CD28RE but not the upstream nuclear factor kappabeta-binding site in the IL-2 promoter reduced B7-1-driven transcription >90%. The results implicates a major role of the CD28RE in the integration of p65/c-Jun-mediated transcription within the IL-2 promoter. We suggest that the transition from an autocrine LFA-3-driven immune response to a B7--induced paracrine immune response involves the activation of c-Jun and p65, which target the CD28RE region of the IL-2 promoter. |
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Authors:
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E Parra; K McGuire; G Hedlund; M Dohlsten |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Journal of immunology (Baltimore, Md. : 1950) Volume: 160 ISSN: 0022-1767 ISO Abbreviation: J. Immunol. Publication Date: 1998 Jun |
Date Detail:
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Created Date: 1998-06-11 Completed Date: 1998-06-11 Revised Date: 2008-11-21 |
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: 5374-81 Citation Subset: AIM; IM |
Affiliation:
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Department of Cell and Molecular Biology, University of Lund, Sweden. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Adjuvants, Immunologic
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physiology Animals Antigens, CD28 / genetics* Antigens, CD58 / physiology Antigens, CD80 / physiology* CHO Cells Cricetinae Drug Synergism Gene Expression Regulation / immunology Genes, Reporter / immunology Humans Interleukin-2 / biosynthesis, genetics* Jurkat Cells Lymphocyte Activation / genetics* NF-kappa B / biosynthesis*, genetics, physiology Promoter Regions, Genetic / immunology* Proto-Oncogene Proteins c-jun / biosynthesis*, physiology Superantigens / physiology T-Lymphocytes / immunology, metabolism Transcription Factor AP-1 / genetics Transcription Factor RelA Transcription, Genetic / immunology Transfection / immunology Up-Regulation / genetics, immunology |
| Chemical | |
Reg. No./Substance:
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0/Adjuvants, Immunologic; 0/Antigens, CD28; 0/Antigens, CD58; 0/Antigens, CD80; 0/Interleukin-2; 0/NF-kappa B; 0/Proto-Oncogene Proteins c-jun; 0/Superantigens; 0/Transcription Factor AP-1; 0/Transcription Factor RelA |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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