ENFORCED BCL2 EXPRESSION IN B-LYMPHOID CELLS PROLONGS ANTIBODY-RESPONSES AND ELICITS AUTOIMMUNE-DISEASE
- Author(s)
- Strasser, A; Whittingham, S; Vaux, DL; Bath, ML; Adams, JM; Cory, S; Harris, AW;
- Details
- Publication Year 1991-10,Volume 88,Issue #19,Page 8661-8665
- Journal Title
- PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
- Publication Type
- Journal Article
- 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.
- Publisher
- NATL ACAD SCIENCES
- Keywords
- HUMAN FOLLICULAR LYMPHOMA; TRANSGENIC MICE; CHROMOSOMAL BREAKPOINT; MEMBRANE PROTEIN; DEREGULATED BCL2; C-MYC; GENE; GROWTH; TRANSLOCATION; SURVIVAL
- Publisher's Version
- https://doi.org/10.1073/pnas.88.19.8661
- Terms of Use/Rights Notice
- Refer to copyright notice on published article.
Creation Date: 1991-10-01 12:00:00