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.
|Number of pages||6|
|Journal||Proceedings of the National Academy of Sciences of the United States of America|
|Publication status||Published - 2 Apr 2002|