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B Is Redundant with p50 During B Cell Proliferative Responses, and Is Required for Germline CH Transcription and Class Switching to IgG31
*
Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139;
Division of Emergency Medicine, Children’s Hospital, Boston, MA 02115; and
Department of Pathology and
§
Biomedical Instrumentation Center, Uniformed Services University of the Health Sciences, Bethesda, MD 20814.
B cells lacking individual NF-
B/Rel family members exhibit
defects in activation programs. We generated small resting B cells
lacking p65 or p50 alone, or lacking both p50 and p65, then evaluated
the ability of these cells to proliferate, secrete Ig, and undergo Ig
class switching. B cells lacking p65 proliferated well in response to
all stimuli tested. However, these cells demonstrated an isolated
defect in switching to IgG3, which was associated with a decrease in
3 germline CH gene expression. Whereas, previously
reported, B cells lacking p50 alone had a severe proliferative defect
in response to LPS, a moderate defect in response to CD40 ligand
(CD40L), and normal proliferation to Ag receptor cross-linking using
dextran-conjugated anti-IgD Abs (
-dex), B cells lacking both
p50 and p65 exhibited severely impaired proliferation in response to
LPS, -dex, and CD40L. This defect could be overcome by
simultaneous administration of -dex and CD40L. In response to
this latter combination of stimuli, B cells lacking both p50 and p65
secreted Ig and underwent isotype switching to IgG1 as efficiently as B
cells lacking p50 alone. These data demonstrate a role for the p65
subunit of NF-B in germline CH gene expression as well
as functional redundancy between p50 and p65 during proliferative
responses.
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