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Prepublished online as a Blood First Edition Paper on October 17, 2002; DOI 10.1182/blood-2002-09-2681. This Article Full Text Full Text (PDF) All Versions of this Article: 2002-09-2681v1 101/5/1913    most recent 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 Manel, N. Articles by Sitbon, M. Search for Related Content PubMed PubMed Citation Articles by Manel, N. Articles by Sitbon, M. Related Collections Immunobiology Cell Cycle Gene Expression Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 1 March 2003, Vol. 101, No. 5, pp. 1913-1918 IMMUNOBIOLOGY The HTLV receptor is an early T-cell activation marker whose expression requires de novo protein synthesis Nicolas Manel, Sandrina Kinet, Jean-Luc Battini, Felix J. Kim, Naomi Taylor, and Marc Sitbon From the Institut de Génétique Moléculaire de Montpellier, CNRS UMR 5535/IFR 24, F-34293 Montpellier Cedex 5, France. The human T-cell leukemia virus type 1 (HTLV) is the first isolated human retrovirus, but its receptor has yet to be identified, in part due to its ubiquitous expression. Here we report that quiescent CD4 and CD8 T lymphocytes do not express this receptor, as monitored with a soluble receptor-binding domain derived from the HTLV envelope. However, HTLV receptor is an early activation marker in neonatal and adult T lymphocytes, detected as early as 4 hours following T-cell-receptor (TCR) stimulation. This induced surface expression of the HTLV receptor requires de novo protein synthesis and results in a wide distribution on the surface of activated lymphocytes. Moreover, the distribution of the HTLV receptor is independent of TCR/CD3-capped membrane structures, as observed by confocal immunofluorescence microscopy. To determine whether HTLV receptor up-regulation specifically requires TCR-mediated signals or, alternatively, is dependent on more generalized cell cycle entry/proliferation signals, its expression was monitored in interleukin 7 (IL-7)-stimulated neonatal and adult T cells. Neonatal, but not adult, lymphocytes proliferate in response to IL-7 and HTLV receptor expression is restricted to the former population. Thus, HTLV receptor expression appears to be an early marker of cell cycle entry. Up-regulation of the HTLV receptor, via signals transmitted through the IL-7 cytokine receptor as well as the TCR, is likely to contribute to the mother-to-infant transmission and spreading of HTLV-1. © 2003 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: M. Lavanya, S. Kinet, A. Montel-Hagen, C. Mongellaz, J.-L. Battini, M. Sitbon, and N. Taylor Cell Surface Expression of the Bovine Leukemia Virus-Binding Receptor on B and T Lymphocytes Is Induced by Receptor Engagement J. Immunol., July 15, 2008; 181(2): 891 - 898. [Abstract] [Full Text] [PDF] N. Takenouchi, K. S. Jones, I. Lisinski, K. Fugo, K. Yao, S. W. Cushman, F. W. Ruscetti, and S. Jacobson GLUT1 Is Not the Primary Binding Receptor but Is Associated with Cell-to-Cell Transmission of Human T-Cell Leukemia Virus Type 1 J. Virol., February 1, 2007; 81(3): 1506 - 1510. [Abstract] [Full Text] [PDF] L. 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