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 Blood, 15 December 2008, Vol. 112, No. 13, pp. 5063-5073.
Prepublished online as a Blood First Edition Paper on September 19, 2008; DOI 10.1182/blood-2007-10-120832.

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IMMUNOBIOLOGY

NF-{kappa}B1 and c-Rel cooperate to promote the survival of TLR4-activated B cells by neutralizing Bim via distinct mechanisms

Ashish Banerjee1, Raelene Grumont1, Raffi Gugasyan1, Christine White2, Andreas Strasser1, and Steve Gerondakis1

1 Walter and Eliza Hall Institute of Medical Research, Parkville, Australia; and 2 Department of Molecular Genetics, Cleveland Clinic, OH

The nuclear factor-{kappa}B (NF-{kappa}B) pathway is crucial for the survival of B cells stimulated through Toll-like receptors (TLRs). Here, we show that the heightened death of TLR4-activated nfkb1–/– B cells is the result of a failure of the Tpl2/MEK/ERK pathway to phosphorylate the proapo-ptotic BH3-only protein Bim and target it for degradation. ERK inactivation of Bim after TLR4 stimulation is accompanied by an increase in A1/Bim and Bcl-xL/Bim complexes that we propose represents a c-Rel–dependent mechanism for neutralizing Bim. Together these findings establish that optimal survival of TLR4-activated B cells depends on the NF-{kappa}B pathway neutralizing Bim through a combination of Bcl-2 prosurvival protein induction and Tpl2/ERK-dependent Bim phosphorylation and degradation.


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