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Blood, 15 December 2005, Vol. 106, No. 13, pp. 4234-4240. Prepublished online as a Blood First Edition Paper on August 30, 2005; DOI 10.1182/blood-2005-05-1871. This Article Full Text (PDF) All Versions of this Article: 2005-05-1871v1 106/13/4234    most recent Alert me when this article is cited Alert me if a correction is posted 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 Leveen, P. Articles by Karlsson, S. Search for Related Content PubMed PubMed Citation Articles by Leveen, P. Articles by Karlsson, S. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted May 9, 2005 Accepted August 13, 2005 TGF- type II receptor deficient thymocytes develop normally but demonstrate increased CD8+ proliferation in vivo Per Leveen, Maria Carlsen, Anna White-Makowska, Saemundur Oddsson, Jonas Larsson, Marie-Jose Goumans, Corrado M Cilio*, and Stefan Karlsson Molecular Medicine and Gene Therapy, Institute of Laboratory Medicine and The Lund Strategic Research Center for Stem Cell Biology and Cell Therapy, Lund University, Lund, Sweden Dept. of Clinical Sciences, Cellular Autoimmunity Unit,, Malmo University Hospital, Lund University, Malmo, Sweden Netherlands Cancer Institute, Amsterdam, The Netherlands * Corresponding author; email: corrado.cilio{at}med.lu.se. We have taken advantage of the Cre/lox system to generate a mouse model with inducible deficiency of transforming growth factor receptor II (TRII). Using this approach, transforming growth factor (TGF-) signaling deficiency can be restricted to the hematopoietic system by bone marrow transplantation. Mice transplanted with TRII -/- bone marrow develop a lethal inflammatory disorder closely resembling that of TGF-1 null mice. Previous in vitro studies have suggested multiple roles for TGF- in T cell development, including proliferation, apoptosis and differentiation. We used our transplantation model to ask whether T cell development is normal in the absence of TGF- signaling. The findings show for the first time in vivo and in foetal thymus organ culture (FTOC) that TGF- is not required for thymocytes to differentiate along the entire pathway of thymic T cell development, as defined by the expression patterns of CD4, CD8, CD25 and CD44. In contrast to previous investigations, no increase of thymocyte apoptosis was observed. However, TRII deficient CD8+ thymocytes displayed a two-fold increase in proliferation rate, as determined by BrdU incorporation in vivo. These results reinforce the importance of TGF- as an immune regulator critical for T cell function. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: R. Tiedt, H. Hao-Shen, M. A. Sobas, R. Looser, S. Dirnhofer, J. Schwaller, and R. C. Skoda Ratio of mutant JAK2-V617F to wild-type Jak2 determines the MPD phenotypes in transgenic mice Blood, April 15, 2008; 111(8): 3931 - 3940. [Abstract] [Full Text] [PDF] D. Pan, T. Schomber, C. P. Kalberer, L. M. Terracciano, K. Hafen, W. Krenger, H. Hao-Shen, C. Deng, and R. C. Skoda Normal erythropoiesis but severe polyposis and bleeding anemia in Smad4-deficient mice Blood, October 15, 2007; 110(8): 3049 - 3055. [Abstract] [Full Text] [PDF]

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