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Regulation of Developing B Cell Survival by RelA-Containing NF-B Complexes ¹

Department of Biological Sciences, Columbia University, New York, NY 10027

Mice deficient in the RelA (p65) subunit of NF-B die during embryonic development. Fetal liver (FL) hemopoietic precursors from these mice were used to generate RelA-deficient lymphocytes by adoptive transfer into lethally irradiated mature lymphocyte-deficient recombination-activating gene-1^-/- mice. Strikingly, RelA^-/- lymphocyte generation was greatly diminished compared with that of RelA^+/+ lymphocytes. The most dramatic reduction was noticed in the numbers of developing B cells, which were considerably increased when RelA^-/- FL cells that were also TNFR1 deficient were used. The role of RelA was further investigated in FL-derived developing B cells in vitro. Our results show that RelA is a major component of constitutive and TNF--induced B site-binding activity in developing B cells, and provide evidence for a direct role of TNF- in killing RelA^-/- B cells. The absence of RelA significantly reduced mRNA expression of the antiapoptotic genes cellular FLICE-inhibitory protein and Bcl-2. Retroviral transduction of RelA^-/- B cells with either cFLIP or Bcl-2 significantly reduced TNF- killing. Together, these results indicate that RelA plays a crucial role in regulating developing B cell survival by inhibiting TNF- cytotoxicity.

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