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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.
Submitted May 22, 2006
Graduate Institute of Immunology, National Taiwan University College of Medicine * Corresponding author; email: leeck{at}ha.mc.ntu.edu.tw.
Transcription factors are critical for instructing the development of B lymphocytes from multipotential progenitor cells in the bone marrow (BM). Here, we showed that 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 periphery. The reduction in the B cell compartment included a reduced percentage and number of pro-B, pre-B, and immature B cells in the absence of STAT3, while 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, due to a decreased number of IL-7 responsive cells rather than to decreased expression or signaling of IL-7R
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| Copyright © 2006 by American Society of Hematology Online ISSN: 1528-0020 | |||||||||
. Moreover, STAT3-deficient mice displayed enhanced apoptosis in the pro-B population when deprived of survival factors, suggesting that at least two mechanisms (impaired differentiation and enhanced apoptosis) are involved in the mutant phenotype. Lastly, BM transplantation confirmed that impaired B lymphopoiesis in the absence of STAT3 was due to 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.
