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This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by da Rocha Dias, S. Articles by Rudd, C. E. Search for Related Content PubMed PubMed Citation Articles by da Rocha Dias, S. Articles by Rudd, C. E. Related Collections Immunobiology Apoptosis Signal Transduction Brief Reports Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 15 February 2001, Vol. 97, No. 4, pp. 1134-1137 BRIEF REPORT CTLA-4 blockade of antigen-induced cell death Silvy da Rocha Dias and Christopher E. Rudd From the Division of Tumor Immunology, Department of Cancer Immunology and AIDS, Dana-Farber Cancer Institute, and Department of Pathology, Harvard Medical School, Boston, MA. While cytotoxic T lymphocyte antigen-4 (CTLA-4) negatively regulates T-cell receptor (TCR)-driven interleukin (IL)-2 production and proliferation, little is known regarding whether the coreceptor has the capacity to inhibit other events, such as Fas ligand (FasL) expression and antigen-induced cell death (AICD). In this study, it is shown that CTLA-4 expressed in a T-cell hybridoma can elicit a potent block of FasL expression and AICD. Inhibition occurred independently of CTLA-4 blockage of IL-2 production and was partially reversed by a single mutation in the cytoplasmic YVKM motif. These findings indicate that CTLA-4 can block TCR signaling prior to bifurcation of signals leading to IL-2 production and apoptosis. © 2001 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: S. Mukherjee, A. Ahmed, S. Malu, and D. Nandi Modulation of cell cycle progression by CTLA4-CD80/CD86 interactions on CD4+ T cells depends on strength of the CD3 signal: critical role for IL-2 J. Leukoc. Biol., July 1, 2006; 80(1): 66 - 74. [Abstract] [Full Text] [PDF] D. Homann, W. Dummer, T. Wolfe, E. Rodrigo, A. N. Theofilopoulos, M. B. A. Oldstone, and M. G. von Herrath Lack of Intrinsic CTLA-4 Expression Has Minimal Effect on Regulation of Antiviral T-Cell Immunity J. Virol., January 1, 2006; 80(1): 270 - 280. [Abstract] [Full Text] [PDF] S. Mukherjee, A. Ahmed, and D. Nandi CTLA4-CD80/CD86 interactions on primary mouse CD4+ T cells integrate signal-strength information to modulate activation with Concanavalin A J. Leukoc. Biol., July 1, 2005; 78(1): 144 - 157. [Abstract] [Full Text] [PDF] T. J. Dillon, K. D. Carey, S. A. Wetzel, D. C. Parker, and P. J. S. Stork Regulation of the Small GTPase Rap1 and Extracellular Signal-Regulated Kinases by the Costimulatory Molecule CTLA-4 Mol. Cell. Biol., May 15, 2005; 25(10): 4117 - 4128. [Abstract] [Full Text] [PDF] S. Sehra, D. Patel, S. Kusam, Z.-Y. Wang, C.-H. Chang, and A. L. Dent A Role for Caspases in Controlling IL-4 Expression in T Cells J. Immunol., March 15, 2005; 174(6): 3440 - 3446. [Abstract] [Full Text] [PDF] P. Pandiyan, D. Gartner, O. Soezeri, A. Radbruch, K. Schulze-Osthoff, and M. C. Brunner-Weinzierl CD152 (CTLA-4) Determines the Unequal Resistance of Th1 and Th2 Cells against Activation-induced Cell Death by a Mechanism Requiring PI3 Kinase Function J. Exp. Med., March 15, 2004; 199(6): 831 - 842. [Abstract] [Full Text] [PDF]

	Copyright © 2001 by American Society of Hematology         Online ISSN: 1528-0020