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Enforced BCL2 expression in B-lymphoid cells prolongs antibody responses and elicits autoimmune disease.
Open accessAbstract
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 (E mu). Mice of a representative transgenic strain, E mu-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 E mu-bcl-2-22 mice constitute a transgenic model for a systemic autoimmune disease resembling the human disorder systemic lupus erythematosus.
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Self-citationApoptosis in the Pathogenesis and Treatment of Disease
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Self-citationLoss of programmed cell death 4 induces apoptosis by promoting the translation of procaspase-3 mRNA
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Protein phosphatase subunit G5PR is needed for inhibition of B cell receptor-induced apoptosis
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Metadata
- Authors
- Strasser, A., Whittingham, S., Vaux, D. L., Bath, M. L., Adams, J. M., Cory, S., & Harris, A. W.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 1991-10
- Volume
- 88
- Issue
- 19
- Pages
- 8661-8665
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W1965322366
- Cited by
- 862
- References
- 2
- FWCI
- 34.99
- Type
- journal article
- Language
- en
- Open access
- green
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