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Age-Related Alterations in the Lymphohematopoietic and B-Lineage Precursor Populations in NZB Mice

^a Division of Rheumatology/Allergy and Clinical Immunology, University of California at Davis, Davis, California, USA;
^b Institute of Bio-Active Science, Nippon Zoki Pharmaceutical Co., Ltd., Kinashi, Hyogo, Japan;
^c The Jackson Laboratory, Bar Harbor, Maine, USA;
^d Department of Pathology and Laboratory Medicine and Josson Comprehensive Cancer Center, School of Medicine, University of California, Los Angeles, California, USA;
^e Department of Pathology, Emory University School of Medicine, Atlanta, Georgia, USA;
^f First Department of Pathology, Transplantation Center, Kansai Medical University, Moriguchi, Osaka, Japan

Key Words. Autoimmunity • B lymphocytes • IL-7R • Pro-B cells • Aging B cells • NZB mice

M. Eric Gershwin, M.D., Division of Rheumatology/Allergy and Clinical Immunology, University of California at Davis, TB 192, One Shields Avenue, Davis, California 95616, USA. Telephone: 530-752-2884; Fax: 530-752-4669; e-mail: megershwin{at}ucdavis.edu

Significant disturbances in B lineage populations of New Zealand Black (NZB) mice have been reported, both with respect to their phenotypes as well as to their function. Notably, there is a profound age-dependent decrease in B-cell precursors in this strain of lupus prone mice. In efforts to characterize the impact of this disturbance in disease, we performed an intensive phenotypic and B-cell population analysis in young and old NZB mice. Our results revealed that there was a significant age-dependent decrease in B cell precursors at all levels of the B-cell-lineage developmental pathway. Analysis of the proliferative capacity of these cell populations showed a comparative decrease in cycling activity in the B-cell-lineage populations of old NZB mice. Furthermore, these cell subsets were much more susceptible to spontaneous apoptosis when compared with similar populations from age-matched BALB/c or young NZB mice. Since the frequency of cells that express the interleukin-7 receptor (IL-7R) declines as NZB mice age, we hypothesize that impairment of IL-7R signal transduction pathways could contribute to severe perturbations of B-cell function in aged NZB mice.