The combined absence of NF-κB1 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

Thomas Pohl, Raffi Gugasyan, Raelene J. Grumont, Andreas Strasser, Donald Metcalf, David Tarlinton, William Sha, David Baltimore, Steve Gerondakis

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Transcription factors NF-κB1 and c-Rel, individually dispensable during embryogenesis, serve similar, yet distinct, roles in the function of mature hemopoietic cells. Redundancy among Rel/ NF-κB family members prompted an examination of the combined roles of c-Rel and NF-κB1 by using mice that lack both proteins. Embryonic development and the maturation of hemopoietic progenitors were unaffected in nfkb1-/-cc-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-1-B cells to proliferate was caused by a cell cycle defect in early G1 that prevented growth. In vivo, defects in humoral immunity and splenic architecture seen in nfkb1-/- and c-rel-/- mice were exacerbated in the double mutant mice. These findings demonstrate that in the B lineage overlapping roles for NF-κB1 and c-Rel appear to be restricted to regulating the activation and function of mature cells.

Original languageEnglish
Pages (from-to)4514-4519
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Issue number7
Publication statusPublished - 2 Apr 2002
Externally publishedYes

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