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Department of Genetics and Pathology, Uppsala University, Uppsala, Sweden
Mice immunized with IgE/Ag complexes produce significantly more
Ag-specific Abs than mice immunized with Ag alone. The enhancement is
mediated via the low-affinity receptor for IgE (Fc
RII or CD23), as
shown by its complete absence in mice pretreated with mAbs specific for
CD23 and in CD23-deficient mice. Because the constitutive expression of
murine CD23 is limited to B cells and follicular dendritic cells
(FDCs), one of these cell types is likely to be involved. One of the
suggested modes of action of IgE/CD23 is to increase the ability of B
cells to present Ag to T cells, as demonstrated to take place in vitro.
Another possibility is that FDCs capture the IgE/Ag complexes and
present these directly to B cells. The purpose of the present study was
to determine whether CD23+ B cells or FDCs are responsible
for the IgE/CD23-mediated enhancement of specific Ab responses in vivo.
We show that the enhancement is completely restored in irradiated
CD23-deficient mice reconstituted with CD23+ spleen or bone
marrow cells. In these mice, the B cells are CD23+ and the
FDCs are presumably CD23- because the FDCs are radiation
resistant and are reported not to be replaced by donor cells after this
type of cell transfer. In contrast, enhancement was not restored in
irradiated wild-type mice reconstituted with CD23- cells.
These results indicate that CD23+ B cells, and not FDCs,
are the cells that capture IgE/Ag complexes and induce
enhancement of Ab responses in vivo.
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