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Blood, 4 June 2009, Vol. 113, No. 23, pp. 5793-5800. Prepublished online as a Blood First Edition Paper on April 8, 2009; DOI 10.1182/blood-2008-12-192252. This Article Full Text Full Text (PDF) Supplemental Figures All Versions of this Article: blood-2008-12-192252v1 113/23/5793    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 CrossRef Google Scholar Articles by Saini, M. Articles by Seddon, B. PubMed PubMed Citation Articles by Saini, M. Articles by Seddon, B. Related Collections Immunobiology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Regulation of T cell-dendritic cell interactions by IL-7 governs T-cell activation and homeostasis Manoj Saini1, Claire Pearson2, and Benedict Seddon2 1 Medical Research Council (MRC) Centre for Immune Regulation, Division of Immunity and Infection, Birmingham University, Birmingham; and 2 Division of Immune Cell Biology, MRC National Institute for Medical Research, London, United Kingdom Interleukin-7 (IL-7) plays a central role in the homeostasis of the T-cell compartment by regulating T-cell survival and proliferation. Whether IL-7 can influence T-cell receptor (TCR) signaling in T cells remains controversial. Here, using IL-7–deficient hosts and TCR-transgenic T cells that conditionally express IL-7R, we examined antigen-specific T-cell responses in vitro and in vivo to viral infection and lymphopenia to determine whether IL-7 signaling influences TCR-triggered cell division events. In vitro, we could find no evidence that IL-7 signaling could costimulate T-cell activation over a broad range of conditions, suggesting that IL-7 does not directly tune TCR signaling. In vivo, however, we found an acute requirement for IL-7 signaling for efficiently triggering T-cell responses to influenza A virus challenge. Furthermore, we found that IL-7 was required for the enhanced homeostatic TCR signaling that drives lymphopenia-induced proliferation by a mechanism involving efficient contacts of T cells with dendritic cells. Consistent with this, saturating antigen-presenting capacity in vivo overcame the triggering defect in response to cognate peptide. Thus, we demonstrate a novel role for IL-7 in regulating T cell–dendritic cell interactions that is essential for both T-cell homeostasis and activation in vivo. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

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