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Molecular & Cellular Proteomics 4:1876-1887, 2005.
© 2005 by The American Society for Biochemistry and Molecular Biology, Inc.

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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.

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