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Published April 2, 2002 | Published
Journal Article Open

The combined absence of NF-kappa B1 and c-Rel reveals that overlapping roles for these transcription factors in the B cell lineage are restricted to the activation and function of mature cells

Abstract

Transcription factors NF-KB1 and c-Rel, individually dispensable during embryogenesis, serve similar, yet distinct, roles in the function of mature hemopoietic cells. Redundancy among Rel/ NF-KB family members prompted an examination of the combined roles of c-Rel and NF-KB1 by using mice that lack both proteins. Embryonic development and the maturation of hemopoietic progenitors were unaffected in nfkb1(-/-)c-rel(-/-) mice. Peripheral T cell populations developed normally, but follicular, marginal zone, and CD5(+) peritoneal B cell populations all were reduced. In culture, a failure of mitogen-stimulated nfkb1(-/-)c-rel(-/-) B cells to proliferate was caused by a cell cycle defect in early G(1) that prevented growth. In vivo, defects in humoral immunity and splenic architecture seen in nfkbl(-/-) and c-rel(-/-) mice were exacerbated in the double mutant mice. These findings demonstrate that in the B lineage overlapping roles for NF-K81 and c-Rel appear to be restricted to regulating the activation and function of mature cells.

Additional Information

© 2002 by the National Academy of Sciences. Communicated by Gustav J. Nossal, University of Melbourne, Melbourne, Australia, February 7, 2002 (received for review October 24, 2001). This work was supported by the National Health and Medical Research Council (Australia), the Anti-Cancer Council of Victoria, and the Leukemia and Lymphoma Society of America.

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