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STAT6, NF-kappaB and C/EBP in CD23 expression and IgE production
S B Tinnell1, S M Jacobs-Helber, E Sterneck
1Department of Microbiology and Immunology, Medical College of Virginia Campus of Virginia Commonwealth University, Richmond 23298, USA.
International Immunology
|October 31, 1998
Summary
STAT6 transcription factors bind the CD23 promoter, but other STATs (STAT3/5) can induce CD23 in STAT6-deficient cells. CD23 superinduction involves STAT and NF-kappaB interactions.
Area of Science:
- Immunology
- Molecular Biology
- Transcription Factor Regulation
Background:
- CD23 is a key regulator of B cell function and IgE production.
- STAT6, NF-kappaB (p50), and C/EBPbeta are transcription factors potentially involved in CD23 regulation.
Purpose of the Study:
- To investigate the roles of STAT6, NF-kappaB (p50), and C/EBPbeta in CD23 gene regulation.
- To elucidate the mechanisms underlying CD23 superinduction.
Main Methods:
- Electrophoretic mobility shift assay (EMSA) to assess transcription factor binding.
- Analysis of knockout mice (STAT6-/-, p50-/-, C/EBPbeta-/-) for CD23 expression and IgE production.
- Western blot analysis to detect protein presence in nuclear extracts.
Main Results:
- STAT6 binds the CD23a promoter with lower affinity.
- STAT6 deficiency leads to reduced CD23 expression upon CD40 ligand stimulation, but CD23 and IgE are induced by CD40 ligand/IL-4.
- STAT3 and STAT5 were found to induce CD23 in STAT6-/- B cells.
- NF-kappaB (p50) is not essential for CD23 induction or IgE production.
- C/EBPbeta does not play a role in CD23 induction but affects IgE production and B cell proliferation.
Conclusions:
- CD23 superinduction is mediated by the interaction of STAT and NF-kappaB transcription factors.
- STAT3 and STAT5 can compensate for STAT6 in CD23 induction under specific conditions.