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Mice lacking the c-rel proto-oncogene exhibit defects in lymphocyte proliferation, humoral immunity, and interleukin-2 expression.
Open accessAbstract
The c-rel proto-oncogene, which is expressed predominantly in hemopoietic cells encodes a subunit of the NF-kappa B-like family of transcription factors. In mice with an inactivated c-rel gene, whereas development of cells from all hemopoietic lineages appeared normal, humoral immunity was impaired and mature B and T cells were found to be unresponsive to most mitogenic stimuli. Phorbol ester and calcium ionophore costimulation, in contrast to certain membrane receptor-mediated signals, overcame the T cell-proliferative defect, demonstrating that T cell proliferation occurs by Rel-dependent and -independent mechanisms. The ability of exogenous interleukin-2 to restore T Cell, but not B cell, proliferation indicates that Rel regulates the expression of different genes in B and T cells that are crucial for cell division and immune function.
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Metadata
- Authors
- Köntgen, F., Grumont, R. J., Strasser, A., Metcalf, D., Li, R., Tarlinton, D., & Gerondakis, S.
- Venue
- Genes & Development
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 1995-08-15
- Volume
- 9
- Issue
- 16
- Pages
- 1965-1977
- ISSN
- 0890-9369 (ISSN-L)
- 1549-5477
- OpenAlex
- W2096589599
- Cited by
- 727
- References
- 1
- Type
- posted content
- Language
- en
- Open access
- diamond
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