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Cited by 862

The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.

Enforced BCL2 expression in B-lymphoid cells prolongs antibody responses and elicits autoimmune disease.

Open access
Strasser, A, Whittingham, S, Vaux, D L, Bath, M L, Adams, J M, Cory, S, Harris, A W·1991·Proceedings of the National Academy of Sciences

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 (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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Crossref · 10.1073/pnas.88.19.8661

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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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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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