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B
and IBß and Sustained Activation of Nuclear Factor-B/c-Rel
*
Department of Internal Medicine and Interdisciplinary Immunology Program, University of Iowa College of Medicine, Iowa City, IA 52242; and
Department of Veterans Affairs, Iowa City, IA 52246
Unmethylated CpG dinucleotides in particular base contexts in
oligonucleotides (CpG DNA) rescue WEHI-231 cells from
anti-IgM-induced cell cycle arrest and apoptosis. Anti-IgM rapidly
elevated the levels of NF
B p50/c-Rel heterodimers followed by a
decline of p50/c-Rel heterodimers by 3 h and a concomitant
increase of p50/p50 homodimers. In contrast, CpG DNA induced and
maintained the levels of p50/c-Rel heterodimers in the presence or
absence of anti-IgM, while control non-CpG DNA failed to induce
NFB activation. Anti-IgM induced IB
degradation followed by
increased IB protein levels. The levels of IBß were
increased after anti-IgM treatment. In contrast, CpG DNA, but not
non-CpG DNA, induced sustained IB and IBß degradation in the
presence or absence of anti-IgM. Inhibition of IB degradation
blocked CpG DNA-induced NFB activation and expression of
c-myc. Prevention of NFB activation by inhibiting
IB degradation also suppressed the ability of CpG DNA to rescue
WEHI-231 cells from anti-IgM-induced apoptosis. These results
indicate that CpG DNA-mediated sustained activation of NFB depends
on the degradation of IB and IBß and is required for the CpG
DNA-mediated anti-apoptosis gene expression and the protection
against anti-IgM-induced apoptosis of WEHI-231 cells.
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