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Enforced BCL2 Expression in B-Lymphoid Cells Prolongs Antibody Responses and Elicits Autoimmune Disease

Andreas Strasser, Senga Whittingham, David L. Vaux, Mary L. Bath, Jerry M. Adams, Suzanne Cory and Alan W. Harris
Proceedings of the National Academy of Sciences of the United States of America
Vol. 88, No. 19 (Oct. 1, 1991), pp. 8661-8665
Stable URL: http://www.jstor.org/stable/2358000
Page Count: 5
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Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
Enforced BCL2 Expression in B-Lymphoid Cells Prolongs Antibody Responses and Elicits Autoimmune Disease
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Abstract

The biological functions of the BCL2 gene were investigated in transgenic mice harboring human BCL2 cDNA under the control of an immunoglobulin heavy chain enhancer (Eμ). Mice of a representative transgenic strain, Eμ-bcl-2-22, had a great excess of B lymphocytes, immunoglobulin-secreting cells, and serum immunoglobulins, attributable to increased longevity of B-lineage cells. Pre-B and plasma cells as well as B cells exhibited prolonged survival in culture. Immunized animals produced an amplified and protracted antibody response. Within the first year of life, most mice spontaneously produced antibodies to nuclear antigens, and 60% developed kidney disease, diagnosed as immune complex glomerulonephritis. Thus Eμ-bcl-2-22 mice constitute a transgenic model for a systemic autoimmune disease resembling the human disorder systemic lupus erythematosus.

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