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1 Transgenic Mice1
*
Department of Medical Microbiology and Immunology, University of Goteborg, Goteborg, Sweden; and
Department of Immunology, University of Birmingham Medical School, Birmingham, United Kingdom
The block in the CD80/CD86-CD28/CTLA-4 pathway in CTLA4-H
1
transgenic (Tg) mice results in strongly impaired systemic IgG immunity
and failure to develop germinal center reactions. By contrast, here we
report that mucosal immunity and IgA B cell differentiation are not
affected by this block. We found abundant germinal centers and evidence
of IgA switch differentiation in Peyer’s patches, normal total IgA
levels, and normal numbers of IgA-labeling cells in the gut mucosa. The
distribution of B-1 and B-2 cells and the relative contribution of B-1
cells to the total IgA B cells were similar in Tg and wild-type mice.
Despite this, oral immunizations with keyhole limpet hemocyanin plus
cholera toxin adjuvant failed to stimulate Ag-specific mucosal IgA
responses in CTLA4-H1 Tg mice. This was not due to a lack of
adjuvant activity of cholera toxin in Tg mice, nor was this secondary
to an inability to take up Ag from the gut lumen. Rather,
CD4+ T cells stimulated by oral immunization in Tg
mice appeared to be inappropriately primed, as evidenced by a
significantly reduced level of CD40 ligand and CD44 expression and an
increased expression of CD95 compared to those in wild-type mice. This
study reveals a paradox in the regulation of mucosal IgA responses.
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