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The Journal of Immunology, 1978, 121: 973-977.
Copyright © 1978 by The American Association of Immunologists, Inc.

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Characterization of a B Cell Defect in the NZB Mouse Manifested by an Increased Ratio of Surface IgM to IgD1

P. Cohen2, M. Ziff3 and E. S. Vitetta

From the Departments of Internal Medicine and Microbiology, University of Texas Southwestern Medical School, Dallas, Texas 75235

Abstract

In an effort to define the cellular basis of abnormalities in polyclonal B cell activation previously noted in NZB mice, the surface immunoglobulin (sIg) isotypes of spleen cells from NZB mice were examined. After lactoperoxidase-catalyzed radioiodination, the cell surface immunoglobulins were analyzed by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE). Spleen cells from 8- to 10-week-old NZB mice were found to have an increased ratio of cell surface IgM/IgD compared to cells from 11 control strains. The altered ratio of sIg isotypes was not a consequence of increased proteolytic activity present in NZB cell suspensions or of the presence of cytophilic antibody or autoantibody.

Ontogenetic studies of the sIgM/sIgD (µ/{delta}) ratio on splenocytes from NZB and BALB/c mice revealed that the former cells had higher µ/{delta} ratios as early as 2 weeks after birth. By 4 weeks of age the µ/{delta} ratios were equivalent. Between 4 weeks and 1 year of age, the µ/{delta} ratios on NZB splenocytes remained constant whereas those on BALB/c splenocytes decreased and reached adult levels at 6 weeks.

Footnotes

1 This work was supported by National Institutes of Health Grants AI-11851, AI-12789, and AM-18505.

2 Recipient of an Arthritis Foundation Postdoctoral Fellowship and a Clinical Investigator Award NIAMDD 1K08AM00378.

3 Recipient of a Research Career Award from the United States Public Health Service.




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B. Kotzin, V. Barr, and E Palmer
A large deletion within the T-cell receptor beta-chain gene complex in New Zealand white mice
Science, July 12, 1985; 229(4709): 167 - 171.
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