Originally published In Press as doi:10.1074/mcp.M500194-MCP200 on August 19, 2005.
Molecular & Cellular Proteomics 4:1876-1887, 2005.
© 2005 by The American Society for Biochemistry and Molecular Biology, Inc.
Research
B7/CD28 Costimulation of T Cells Induces a Distinct Proteome Pattern*
Kai Kronfeld , ,
Elisabeth Hochleitner¶,
Simone Mendler ,||,
Jutta Goldschmidt ,
Rudolf Lichtenfels ,**,
Friedrich Lottspeich¶,
Hinrich Abken and
Barbara Seliger ,**,
From the IIIrd Department of Internal Medicine, Johannes Gutenberg University, 55131 Mainz, Germany, Coordination Centre for Clinical Trials (Koordinationzentrum für Klinische Studien Mainz), Johannes Gutenberg University, 55131 Mainz, Germany, ¶ Max Planck Institute for Biochemistry, 82152 Martinsried, Germany, || Department of Otorhinolaryngology, Johannes Gutenberg University, 55131 Mainz, Germany,  Department I of Internal Medicine, Tumor Genetics and Centre of Molecular Medicine Cologne, University of Cologne, 50924 Cologne, Germany, and ** Institute of Medical Immunology, Martin Luther University Halle-Wittenberg, 06112 Halle, Germany
Effective immune strategies for the eradication of human tumors require a detailed understanding of the interaction of tumor cells with the immune system, which might lead to an optimization of T cell responses. To understand the impact of B7-mediated costimulation on T cell activation comprehensive proteome analysis of B7-primed T cell populations were performed. Using this approach we identified different classes of proteins in T cells whose expression is either elevated or reduced upon B7-1- or B7-2-mediated CD28 costimulation. The altered proteins include regulators of the cell cycle and cell proliferation, signal transducers, components of the antigen processing machinery, transporters, cytoskeletal proteins, and metabolic enzymes. A number of differentially expressed proteins are further modified by phosphorylation. Our results provide novel insights into the complexity of the CD28 costimulatory pathway of T cells and will help to identify potential targets of therapeutic interventions for modulating anti-tumor T cell activation.
 To whom correspondence should be addressed: Inst. of Medical Immunology, Martin Luther University Halle-Wittenberg, Magdeburger Strasse 2, 06112 Halle, Germany. Tel.: 49-345-5-57-40-54; Fax: 49-345-5-57-40-55; E-mail: Barbara.Seliger{at}medizin.uni-halle.de

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Copyright © 2005 by the American Society for Biochemistry and Molecular Biology.
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