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Blood, 15 September 2006, Vol. 108, No. 6, pp. 1949-1956. Prepublished online as a Blood First Edition Paper on May 16, 2006; DOI 10.1182/blood-2006-04-016857. This Article Full Text Full Text (PDF) Supplemental Figures All Versions of this Article: blood-2006-04-016857v1 108/6/1949    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 Buentke, E. Articles by Seddon, B. Search for Related Content PubMed PubMed Citation Articles by Buentke, E. Articles by Seddon, B. Related Collections Immunobiology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Do CD8 effector cells need IL-7R expression to become resting memory cells? Eva Buentke, Anne Mathiot, Mauro Tolaini, James Di Santo, Rose Zamoyska, and Benedict Seddon From the Division of Immune Cell Biology and the Division of Molecular Immunology, National Institute for Medical Research, London, United Kingdom; Institute Pasteur, Paris, France; and Cancercenter Karolinska, Karolinska Hospital, Stockholm, Sweden. The role for IL-7R expression in the differentiation of effector T cells into resting memory remains controversial. Here, using a conditional IL-7R transgenic model, we were able to test directly whether CD8 effector T cells require IL-7R expression for their differentiation into resting memory cells. In the absence of IL-7R expression, effector cells transferred into "full" hosts underwent a protracted and unremitting contraction compared with IL-7R–expressing control cells and were unable to develop into long-term resting memory cells. Surprisingly, when the same effector cells were transferred into empty T-cell–deficient hosts, they could generate long-lived fully functional resting memory cells independently of IL-7R expression. Formation of these latter cells was found to be dependent on IL-15, because the same IL-7R–deficient effector cells were rapidly lost from IL-15–deficient hosts, having a half-life of less than 40 hours. Therefore, our data suggest that, under physiological conditions, both IL-7 and IL-15 synergize to promote the formation of memory cells directly by limiting the contraction of effectors that occurs following an immune response and that reexpression of IL-7R is a key checkpoint in the regulation of this process. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: N. L. Alves, E. M. M. van Leeuwen, I. A. M. Derks, and R. A. W. van Lier Differential Regulation of Human IL-7 Receptor {alpha} Expression by IL-7 and TCR Signaling J. Immunol., April 15, 2008; 180(8): 5201 - 5210. [Abstract] [Full Text] [PDF] C. D. Hammerbeck and M. F. Mescher Antigen Controls IL-7R{alpha} Expression Levels on CD8 T Cells during Full Activation or Tolerance Induction J. Immunol., February 15, 2008; 180(4): 2107 - 2116. [Abstract] [Full Text] [PDF] A. Yates, M. Saini, A. Mathiot, and B. Seddon Mathematical Modeling Reveals the Biological Program Regulating Lymphopenia-Induced Proliferation J. Immunol., February 1, 2008; 180(3): 1414 - 1422. [Abstract] [Full Text] [PDF]

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