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Blood, 15 December 2007, Vol. 110, No. 13, pp. 4367-4369. Prepublished online as a Blood First Edition Paper on September 18, 2007; DOI 10.1182/blood-2007-06-098244. This Article Full Text (PDF) All Versions of this Article: blood-2007-06-098244v1 110/13/4367    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 Kaplan, M. H Articles by Bruns, H. A Search for Related Content PubMed PubMed Citation Articles by Kaplan, M. H Articles by Bruns, H. A Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted June 26, 2007 Accepted September 15, 2007 Constitutively active Stat6 predisposes towards a lymphoproliferative disorder Mark H Kaplan*, Sarita Sehra, Hua-Chen Chang, John T O'Malley, Anubhav N Mathur, and Heather A Bruns Departments of Pediatrics, and Microbiology and Immunology, Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN, United States Department of Biology, Ball State University, Muncie, IN, United States * Corresponding author; email: mkaplan2{at}iupui.edu. Signal Transducer and Activator of Transcription 6 (STAT6) is critical for IL-4 and IL-13 responses, and necessary for the normal development of Th2 cells. We have previously generated mice that express a constitutively active STAT6 (STAT6VT) under control of the CD2 locus control region, which directs expression to the T cell compartment. We now describe that a small proportion of these mice (~5%) develop a spontaneous lymphoproliferative disease (LPD) that results in dramatic splenomegaly. The cell populations observed in the LPD spleens can be divided into two categories, those that are comprised of mixed lineage cells and those that are predominantly T cells with a phenotype similar to that in Autoimmune Lymphoproliferative Syndrome (ALPS) patients. These data suggest that while active Stat6 is not a transforming factor, expression in T cells predisposes towards the development of lymphoproliferative disorders. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: M. Yu, J. L. Moreno, J. P. Stains, and A. D. Keegan Complex Regulation of Tartrate-resistant Acid Phosphatase (TRAP) Expression by Interleukin 4 (IL-4): IL-4 INDIRECTLY SUPPRESSES RECEPTOR ACTIVATOR OF NF-{kappa}B LIGAND (RANKL)-MEDIATED TRAP EXPRESSION BUT MODESTLY INDUCES ITS EXPRESSION DIRECTLY J. Biol. Chem., November 20, 2009; 284(47): 32968 - 32979. [Abstract] [Full Text] [PDF] O. Ritz, C. Guiter, F. Castellano, K. Dorsch, J. Melzner, J.-P. Jais, G. Dubois, P. Gaulard, P. Moller, and K. Leroy Recurrent mutations of the STAT6 DNA binding domain in primary mediastinal B-cell lymphoma Blood, August 6, 2009; 114(6): 1236 - 1242. [Abstract] [Full Text] [PDF]

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