International Immunology Advance Access published online on May 20, 2005
International Immunology, doi:10.1093/intimm/dxh263
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1 Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA; Department of Molecular Biophysics and Biochemistry, Yale University School of Medicine, New Haven, CT 06520, USA
* To whom correspondence should be addressed. The regulation of the transcription factor nuclear factor- *These authors contributed equally to the study.
Received August 20, 2004
Accepted March 24, 2005
Article
Activation of NF-
B promotes the transition of large, CD43+ pre-B cells to small, CD43- pre-B cells
2 Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA; Department of Molecular Biophysics and Biochemistry, Yale University School of Medicine, New Haven, CT 06520, USA; Present address: Department of Physiology, UCLA, Los Angeles, CA 90401, USA
3 Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA; Present address: Department of Medicine, University of Vermont, Burlington, VT 05405, USA
4 Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA; Department of Molecular Biophysics and Biochemistry, Yale University School of Medicine, New Haven, CT 06520, USA; Present address: Institute for Clinical Immunology, Friedrich-Alexander University, Erlangen, Germany
5 Department of Immune Regulation, Tokyo Medical and Dental University, Graduate School of Medicine, Tokyo 113-8519, Japan
6 Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA; Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06520, USA
Sankar Ghosh, E-mail: sankar.ghosh{at}yale.edu
Abstract 
B (NF-B) during B-cell development was examined using cells isolated from the bone marrow of transgenic mice expressing a B luciferase reporter gene. The results indicate that the highest level of NF-B activity is present in cells expressing the pre-B-cell receptor. Furthermore, cross-linking of Ig
on CD43+ pre-B cells is able to activate NF-B in recombination-activating gene 1-deficient mice, preceding their further differentiation into CD43- pre-B cells. Expression of a dominant negative form of IB
using a transgenic approach or by retroviral infection leads to a reduction in the number of CD43+ pre-B cells. These data therefore indicate that activation of NF-B in CD43+ pre-B cells, as a result of signaling by the pre-B-cell receptor, facilitates the continued development of large, CD43+ pre-B cells into small CD43- pre-B cells.
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