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Developmental Immunology
Volume 9, Issue 1, Pages 35-45

Increased Frequency of Pre–Pro B Cells in the Bone Marrow of New Zealand Black (NZB) Mice: Implications for aDevelopmental Block in B Cell Differentiation

1Division of Rheumatology, Allergy and Clinical Immunology, University of California at Davis School of Medicine, TB 192, One Shields Avenue, Davis, CA 95616, USA
2Institute of Bio-Active Science, Nippon Zoki Pharmaceutical Co., Ltd., Kinashi, Yashiro-Cho, Kato-gun, Hyogo 673-1461, Japan
3The Jackson Laboratory, 600 Main Street, Bar Harbor, ME 04609, USA
4Department of Pathology and Laboratory Medicine and Josson Comprehensive Cancer Center, School of Medicine, University of California, Los Angeles, CA 90095, USA
5Department of Pathology, Emory University School of Medicine, Atlanta, GA 30322, USA
6fFirst Department of Pathology, Transplantation Center, Kansai Medical University, Moriguchi, Osaka, Japan

Copyright © 2002 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Reductions in populations of both Pre-B cell (Hardy fractions D) and Pro-B cells (Hardy fractions B–C) have been described in association with murine lupus. Recent studies of B cell populations, based on evaluation of B cell differentiation markers, now allow the enumeration and enrichment of other stage specific precursor cells. In this study we report detailed analysis of the ontogeny of B cell lineage subsets in New Zealand black (NZB) and control strains of mice. Our data suggest that B cell development in NZB mice is partially arrested at the fraction A Pre–Pro B cell stage. This arrest at the Pre-Pro B cell stage is secondary to prolonged lifespan and greater resistance to spontaneous apoptosis. In addition, expression of the gene encoding the critical B cell development transcription factor BSAP is reduced in the Pre–Pro B cell stage in NZB mice. This impairment may influence subsequent B cell development to later stages, and thereby accounts for the down-regulation of the B cell receptor component Igα (mb-1). Furthermore, levels of expression of the Rug2, λ5 and Igβ (B29) genes are also reduced in Pre–Pro B cells of NZB mice. The decreased frequency of precursor B cells in the Pre–Pro B cell population occurs at the most primitive stage of B cell differentiation.