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Department of Microbiology and Immunology, Virginia Commonwealth University, Richmond, VA 23298
CD23, also known as the low affinity IgE receptor (Fc
RII), has
been hypothesized to have a role in IgE regulation. A new CD23
transgenic mouse was generated using the MHC class I promoter and IgH
enhancer to further test the hypothesis that CD23 plays a role in the
down-regulation of IgE. Study of three founder lines by FACS showed
overexpression to varying extents on both B and T lymphocytes. No
alterations in lymphocyte populations was observed. All three founder
lines exhibited strong suppression of IgE in response to DNP-keyhole
limpet hemocyanin/alum and Nippostrongylus brasiliensis
infection compared with that in parental or littermate controls. The
founder line exhibiting the highest level of suppression also was less
susceptible to Ag-induced systemic anaphylactic shock. Overall, the
data support the concept that enhancing CD23 levels can be used to
suppress IgE-mediated disease. The mechanism involves decreased IgE
synthesis, because the serum half-life of IgE was not altered in
transgenics, and enzyme-linked immunospot analysis demonstrated lower
IgE-producing cells stimulated by injection of anti-IgD.
Transgenics also exhibited significantly decreased IgG1 responses and
exhibited lower levels of all Ig isotypes, although this was more
variable in different founder lines.
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