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Updated: Jun 29, 2026

Detection of True IgE-expressing Mouse B Lineage Cells
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129/SvJ mice have mutated CD23 and hyper IgE.

Jill W Ford1, Jamie L Sturgill, Daniel H Conrad

  • 1Virginia Commonwealth University, Department of Microbiology and Immunology, P.O. Box 980678, MCV Station, Richmond, VA 23298, USA.

Cellular Immunology
|October 3, 2008
PubMed
Summary

Mutations in CD23, the low-affinity IgE receptor, were found in 129/SvJ mice. Despite reduced in vitro IgE, these mice showed higher IgE in vivo, suggesting CD23 regulates IgE production.

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Area of Science:

  • Immunology
  • Molecular Biology

Background:

  • CD23 (low-affinity IgE receptor) is proposed to negatively regulate IgE production.
  • Reduced CD23 surface levels were observed in 129/SvJ mice, prompting further investigation.

Purpose of the Study:

  • To investigate the characteristics of CD23 in 129/SvJ mice.
  • To determine the influence of CD23 variations on IgE levels and immune responses.

Main Methods:

  • Sequencing to identify mutations in 129/SvJ CD23.
  • In vitro B cell proliferation assays stimulated with IL-4 and CD40 ligand.
  • Measurement of in vitro IgE levels.
  • In vivo assessment of IgE phenotype and parasite clearance (Nippostrongylus brasiliensis).

Main Results:

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  • Five amino acid substitutions were identified in 129/SvJ CD23, also present in other mouse strains.
  • 129/SvJ B cells exhibited enhanced proliferation but reduced in vitro IgE production.
  • In vivo, 129/SvJ mice displayed a hyper IgE phenotype and faster clearance of Nippostrongylus brasiliensis infection.

Conclusions:

  • CD23 mutations in 129/SvJ mice correlate with a hyper IgE phenotype in vivo.
  • The study reinforces the role of CD23 as a significant regulatory factor in IgE production.
  • Discrepancies between in vitro and in vivo findings highlight the complexity of CD23 regulation.