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Humoral response suppression observed with CD23 transgenics
M E Payet1, E C Woodward, D H Conrad
1Department of Microbiology and Immunology, Virginia Commonwealth University, Richmond 23298, USA.
Journal of Immunology (Baltimore, Md. : 1950)
|June 29, 1999
Summary
This study generated CD23 transgenic mice to investigate its role in IgE regulation. Enhanced CD23 levels effectively suppressed IgE production and reduced allergic reactions, supporting CD23 as a therapeutic target.
Area of Science:
- Immunology
- Molecular Biology
Background:
- CD23, the low affinity IgE receptor (FcεRII), is implicated in IgE regulation.
- Previous hypotheses suggested CD23's role in down-regulating IgE levels.
Purpose of the Study:
- To generate and study CD23 transgenic mice to test its role in IgE down-regulation.
- To evaluate the therapeutic potential of enhancing CD23 expression for IgE-mediated diseases.
Main Methods:
- Generation of CD23 transgenic mice using MHC class I promoter and IgH enhancer.
- Flow cytometry (FACS) to assess CD23 overexpression on lymphocytes.
- Immunological assays to measure IgE, IgG1, and other isotypes in response to allergens and infections.
Main Results:
- Transgenic mice showed varying levels of CD23 overexpression on B and T lymphocytes without altering populations.
- All founder lines exhibited significant suppression of IgE production and reduced susceptibility to anaphylactic shock.
- Decreased IgE synthesis was confirmed, with no change in IgE serum half-life; lower IgG1 and other Ig isotypes were also observed.
Conclusions:
- Enhancing CD23 levels effectively suppresses IgE synthesis and mitigates IgE-mediated allergic responses.
- The data support CD23 as a viable target for therapeutic intervention in IgE-related diseases.