International Immunology Advance Access originally published online on May 20, 2005
International Immunology 2005 17(6):815-825; doi:10.1093/intimm/dxh263
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Activation of NF-
B promotes the transition of large, CD43+ pre-B cells to small, CD43– pre-B cells
1 Section of Immunobiology, 2 Department of Molecular Biophysics and Biochemistry, Yale University School of Medicine, New Haven, CT 06520, USA
3 Department of Immune Regulation, Tokyo Medical and Dental University, Graduate School of Medicine, Tokyo 113-8519, Japan
4 Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06520, USA
5 Present address: Department of Physiology, UCLA, Los Angeles, CA 90401, USA
6 Present address: Department of Medicine, University of Vermont, Burlington, VT 05405, USA
7 Present address: Institute for Clinical Immunology, Friedrich-Alexander University, Erlangen, Germany
Correspondence to: S. Ghosh; E-mail: sankar.ghosh{at}yale.edu
The regulation of the transcription factor nuclear factor-
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 Igß 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.
Keywords: NF-kappa B, B-cells, lymphocytes, development, apoptosis
* These authors contributed equally to the study.
Transmitting editor: W. Leonard
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