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Blood, 1 August 2008, Vol. 112, No. 3, pp. 626-634. Prepublished online as a Blood First Edition Paper on May 12, 2008; DOI 10.1182/blood-2007-10-115618. This Article Full Text Full Text (PDF) Supplemental Table and Figures All Versions of this Article: blood-2007-10-115618v1 112/3/626    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 Citing Articles via Google Scholar Google Scholar Articles by Hauri-Hohl, M. M. Articles by Holländer, G. A. Search for Related Content PubMed PubMed Citation Articles by Hauri-Hohl, M. M. Articles by Holländer, G. A. Related Collections Immunobiology Chemokines, Cytokines, and Interleukins Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY TGF-β signaling in thymic epithelial cells regulates thymic involution and postirradiation reconstitution Mathias M. Hauri-Hohl1, Saulius Zuklys1, Marcel P. Keller1, Lukas T. Jeker1, Thomas Barthlott1, Anne M. Moon2, Jürgen Roes3, and Georg A. Holländer1 1 Laboratory of Pediatric Immunology, Center for Biomedicine, Department of Clinical-Biological Sciences, University of Basel and The University Children's Hospital (UKBB), Basel, Switzerland; 2 Division of Pediatric Critical Care, Utah Health Sciences Center, The University of Utah, Salt Lake City; and 3 Department of Immunology and Molecular Pathology, University College London, London, United Kingdom The thymus constitutes the primary lymphoid organ responsible for the generation of naive T cells. Its stromal compartment is largely composed of a scaffold of different subsets of epithelial cells that provide soluble and membrane-bound molecules essential for thymocyte maturation and selection. With senescence, a steady decline in the thymic output of T cells has been observed. Numeric and qualitative changes in the stromal compartment of the thymus resulting in reduced thymopoietic capacity have been suggested to account for this physiologic process. The precise cellular and molecular mechanisms underlying thymic senescence are, however, only incompletely understood. Here, we demonstrate that TGF-β signaling in thymic epithelial cells exerts a direct influence on the cell's capacity to support thymopoiesis in the aged mouse as the physiologic process of thymic senescence is mitigated in mice deficient for the expression of TGF-βRII on thymic epithelial cells. Moreover, TGF-β signaling in these stromal cells transiently hinders the early phase of thymic reconstitution after myeloablative conditioning and hematopoietic stem cell transplantation. Hence, inhibition of TGF-β signaling decelerates the process of age-related thymic involution and may hasten the reconstitution of regular thymopoiesis after hematopoietic stem cell transplantation. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

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