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Blood, 1 November 2006, Vol. 108, No. 9, pp. 3005-3011. Prepublished online as a Blood First Edition Paper on July 6, 2006; DOI 10.1182/blood-2006-05-024430. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2006-05-024430v1 108/9/3005    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 Chou, W.-C. Articles by Lee, C.-K. Search for Related Content PubMed PubMed Citation Articles by Chou, W.-C. Articles by Lee, C.-K. Related Collections Hematopoiesis and Stem Cells Immunobiology Apoptosis Signal Transduction Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMATOPOIESIS STAT3 positively regulates an early step in B-cell development Wei-Chun Chou, David E. Levy, and Chien-Kuo Lee From the Graduate Institute of Immunology, National Taiwan University College of Medicine, Taipei, Taiwan, Republic of China; and the Departments of Pathology and Microbiology, New York University School of Medicine, New York, NY. Transcription factors are critical for instructing the development of B lymphocytes from multipotential progenitor cells in the bone marrow (BM). Here, we show that the absence of STAT3 impaired B-cell development. Mice selectively lacking STAT3 in BM progenitor cells displayed reduced numbers of mature B cells, both in the BM and in the periphery. The reduction in the B-cell compartment included reduced percentages and numbers of pro-B, pre-B, and immature B cells in the absence of STAT3, whereas the number of pre–pro-B cells was increased. We found that pro-B and pre-B–cell populations lacking STAT3 were hyporesponsive to IL-7 because of a decreased number of IL-7–responsive cells rather than decreased expression or signaling of IL-7R. Moreover, STAT3-deficient mice displayed enhanced apoptosis in the pro-B population when deprived of survival factors, suggesting that at least 2 mechanisms (impaired differentiation and enhanced apoptosis) are involved in the mutant phenotype. Last, BM transplantation confirmed that impaired B lymphopoiesis in the absence of STAT3 was caused by a cell autonomous defect. In sum, these studies defined a specific role for STAT3 in early B-cell development, probably acting at the pre–pro-B transition by contributing to the survival of IL-7–responsive progenitors. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: J. Seita, M. Asakawa, J. Ooehara, S.-i. Takayanagi, Y. Morita, N. Watanabe, K. Fujita, M. Kudo, J. Mizuguchi, H. Ema, et al. Interleukin-27 directly induces differentiation in hematopoietic stem cells Blood, February 15, 2008; 111(4): 1903 - 1912. [Abstract] [Full Text] [PDF]

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