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The Journal of Immunology, 2004, 172: 4159-4166.
Copyright © 2004 by The American Association of Immunologists

Separation of the New Zealand Black Genetic Contribution to Lupus from New Zealand Black Determined Expansions of Marginal Zone B and B1a Cells1

Stephanie Atencio*,{dagger}, Hirofumi Amano{ddagger}, Shozo Izui{ddagger} and Brian L. Kotzin2,*,{dagger}

* Department of Medicine, University of Colorado Health Sciences Center, Denver, CO 80262; {dagger} Integrated Department of Immunology, University of Colorado Health Sciences Center and National Jewish Medical and Research Center, Denver, CO 80262; and {ddagger} Department of Pathology, Centre Medical Universitaire, Geneva, Switzerland

The F1 hybrid of New Zealand Black (NZB) and New Zealand White (NZW) mice develop an autoimmune disease similar to human systemic lupus erythematosus. Because NZB and (NZB x NZW)F1 mice manifest expansions of marginal zone (MZ) B and B1a cells, it has been postulated that these B cell abnormalities are central to the NZB genetic contribution to lupus. Our previous studies have shown that a major NZB contribution comes from the Nba2 locus on chromosome 1. C57BL/6 (B6) mice congenic for Nba2 produce antinuclear Abs, and (B6.Nba2 x NZW)F1 mice develop elevated autoantibodies and nephritis similar to (NZB x NZW)F1 mice. We studied B cell populations of B6.Nba2 mice to better understand the mechanism by which Nba2 leads to disease. The results showed evidence of B cell activation early in life, including increased levels of serum IgM, CD69+ B cells, and spontaneous IgM production in culture. However, B6.Nba2 compared with B6 mice had a decreased percentage of MZ B cells in spleen, and no increase of B1a cells in the spleen or peritoneum. Expansions of these B cell subsets were also absent in (B6.Nba2 x NZW)F1 mice. Among the strains studied, B cell expression of {beta}1 integrin correlated with differences in MZ B cell development. These results show that expansions of MZ B and B1a cells are not necessary for the NZB contribution to lupus and argue against a major role for these subsets in disease pathogenesis. The data also provide additional insight into how Nba2 contributes to lupus.




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