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B Activation by a Distinct Subset of CD40-Mediated Effector Functions in B Lymphocytes1
,
,§
*
Immunology Graduate Program, and Departments of
Microbiology and
Internal Medicine, University of Iowa, Iowa City, IA 52242; and
§
Veterans Affairs Medical Center, Iowa City, IA 52242
CD40 stimulation, which is crucial for generating an effective
T-dependent humoral response, leads to the activation of transcription
factors NF-AT (nuclear factor of activated T cells), AP-1 (activator
protein-1), and NF-
B (nuclear factor-B). However, which
CD40-mediated B cell functions actually require activation of specific
transcription factors is unknown. We examined the causal relationship
between NF-B activation and CD40 effector functions by evaluating
CD40 functions in the presence of an inducible mutant inhibitory
B
(IB) superrepressor. IBAA inhibited nuclear
translocation of multiple NF-B dimers without the complicating
effect of depriving cells of NF-B during development. This approach
complements studies that use mice genetically deficient in single or
multiple NF-B subunits. Interestingly, only a subset of CD40
effector functions was found to require NF-B activation. Both
CD40-induced Ab secretion and B7-1 up-regulation were completely
abrogated by expression of IBAA. Surprisingly, up-regulation of
Fas, CD23, and ICAM-1 was partially independent, and up-regulation of
LFA-1 was completely independent, of CD40-induced NF-B activation.
For the first time, it is clear that distinct transcription factors are
required for the dynamic regulation of CD40
functions.
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